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DISEASES 


BRONCHI,  LUNGS,  AND 
PLEURA 


BY 

FREDERICK  T.  LORD,  M.D. 

VISITING    PHYSICIAN,     MASSACHUSETTS     GENERAL    HOSPITAL;    VISITING     PHYSICIAN,    CHANNING     HOME 
(FOB    CONSUMPTIVES)  ;    INSTRUCTOR    IN     CLINICAL    MEDICINE,     HARVARD     MEDICAL    SCHOOL 


ILLUSTRATED   WITH  93  ENGRAVINGS  AND   3   COLORED  PLATES 


LEA   &   FEBIGER 

PHILADELPHIA    AND   NEW    YORK 
1915 


Entered  according  to  the  Act  of  Congress,  in  the  year  1915,  by 

LEA  &  FEBIGER, 
in  (he  office  of  the  Librarian  of  Congress.      All  rights  reserved. 


1 


TO    THE    MEMORY 


REGINALD  HEBER  FITZ 

VISITING   PHYSICIAN,    MASSACHUSETTS    GENERAL   HOSPITAL 
HERSEY  PROFESSOR  OF   THE  THEORY  AND   PRACTICE  OF  PHYSIC,  HARVARD  UNIVERSITY 

CRITICAL  AND   INSPIRING  TEACHER  WHO 

THROUGH  HIS   SOUND   KNOWLEDGE   OF  PATHOLOGIC   ANATOMY 

MADE   LASTING    CONTRIBUTIONS  TO    MEDICAL  SCIENCE 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

Open  Knowledge  Commons 


http://www.archive.org/details/diseasesofbronchOOIord 


PREFACE 


It  is  hoped  that  the  following  pages  will  fill  the  present  need  of  a 
practical  treatise  on  the  diseases  of  the  respiratory  organs.  The  aim 
has  been  to  present  current  knowledge,  founded  on  the  literature  and 
the  experience  gained  in  the  wards  and  pathologic  laboratory  of  the 
Massachusetts  General  Hospital,  in  such  form  as  to  be  of  value  to 
students  and  practitioners  and  also  to  provide  a  basis  for  further 
research.  References  are  given  to  the  most  important  original  articles 
in  order  that  the  literature  may  be  readily  available  to  those  who  wish 
to  go  more  fully  into  particular  problems.  Pulmonary  tuberculosis 
is  not  considered  under  a  separate  heading,  but  special  attention  is 
given  to  conditions  which  simulate  pulmonary  tuberculosis  and  their 
differential  diagnosis. 

I  am  greatly  indebted  to  Sir  William  Osier  and  Dr.  Thomas  McCrae 
and  to  the  publishers,  Messrs.  Lea  &  Febiger,  for  the  privilege  of  revis- 
ing and  including  in  this  work  the  sections  on  the  diseases  of  the  pleura 
written  for  Osier  and  McCrae's  Modern  Medicine.  It  is  a  pleasure  to 
acknowledge  my  share  in  the  obligation  of  all  students  of  respiratory 
diseases  to  the  publications  of  Dr.  Albert  Fraenkel.  My  thanks  are 
due  to  Dr.  James  Homer  Wright  for  the  use  of  pathologic  material,  to 
Dr.  Walter  J.  Dodd  for  the  a;-ray  plates,  and  to  Mr.  Lewis  S.  Brown 
for  the  photographs. 

F.  T.  L. 

Boston,  Mass.,  1915. 


CONTENTS. 


SECTION    I. 
DISEASES   OF  THE   BRONCHI. 

CHAPTER   I. 

Bronchostenosis -. 17 

1.  Bronchial  Tumors 22 

2.  Syphilis  of  the  Trachea  and  Bronchi 23 

3.  Tuberculosis 27 

4.  Scleroma 28 

5.  Aspirated  Foreign  Bodies 29 

6.  Foreign  Bodies  Arising  from  Within 39 

CHAPTER  II. 

Asthma 44 

CHAPTER  III. 

Bronchitis  Fibrinosa  . .  65 

CHAPTER  IV. 

Bronchitis  Obliterans 74 

CHAPTER  V. 

Bronchitis ; 77 

1.  Acute  Tracheobronchitis 77 

2.  Capillary  Bronchitis  (see  Bronchopneumonia) 94 

3.  Chronic  Bronchitis 94 

CHAPTER  VI. 

Bronchiectasis 10S 

Congenital  Bronchiectasis '126 

(a)  Fetal ^ 126 

(b)  Atelectatic 127 

CHAPTER  VII. 

Bronchial  Blastomycosis 128 


VIII 


I  "\  / ■/■.  \  lis 


-1  <    I  [ON    II. 
D1S1   VS1  S   '  'I     TIN.    LUNGS. 


\  I  M.I  .    I  ISIS 


'  II  \ i *  1 1 : 1 ;   \  ill. 


129 


CHAPTER    IX. 
Emphybi  m  \ 

I    I  diffuse  \  esicular  Emphysema 
■_'.  Acute  Vesicular  Emphysema 
ompensatory  Emphysema 
iilr  EmpbyBema 
5.  [nteratitial  Emphysema 


140 
140 
152 
152 
153 
153 


CHAPTER    X. 
Lobar  Pneumonia.    Obdinabi  Lobab  Pneumonia 


157 


CHAPTER  XI. 
Priedlandeb's  Bacillus  Pneumonia.     . 


234 


CHAPTER  XII. 
Pern  icosis '  241 


CHAPTER    XIII. 


Bbonchopnei  monia 


245 


CHAPTER  XIV. 

Si  BA<  DTE   AND  CHBONIC   InDUBATTVE   PNEUMONIA 


2G4 


CHAPTER  XV. 
I'M. i  MONO!  ONIOSIS 276 


CHAPTER  XVI. 
Pulmonabi   Abscess  and  Gangbene 


290 


CHAPTER    XVII. 


1  '"!'  '  LATOB1     I  >l-Tl  RBANCES 

Pulmonary  <  ingestion 
Active  <  !ongestioo 
-lion 

Pulmonary  Edema 
Chronic  Form   . 
Acute  Form 


318 
318 
318 
319 
321 
322 
322 


CONTENTS  ix 

CHAPTER  XVIII. 
Pulmonary  Thrombosis,  Embolism,  and  Infarction 328 

CHAPTER  XIX. 

Hemoptysis :      .      .      .     352 

CHAPTER  XX. 

Pulmonary  Syphilis 364 

CHAPTER  XXI. 

Pulmonary  Actinomycosis , 371 

CHAPTER  XXII. 
Pulmonary  Streptothricosis 389 

CHAPTER   XXIII. 

Pulmonary  Blastomycosis -.-....     392 

CHAPTER  XXIV. 

Pulmonary  Aspergillosis 399 

CHAPTER  XXV. 

Animal  Parasites 404 

1.  Echinococcus  Disease  of  the  Lung 404 

2.  Pulmonary  Distomatosis  (Lung-fluke  Disease) 420 

3.  Other  Parasites    .      .  ' 426 

CHAPTER  XXVI. 

Tumors  of  the  Bronchi  and  Lung 427 

1.  Benign 427 

2.  Malignant 428 

(a)  Primary  Cancer  of  the  Lung 428 

(b)  Primary  Sarcoma  of  the  Lung 432 

(c)  Secondary  Malignant  Disease  of  the  Lung 446 

CHAPTER  XXVII. 
Lung  Hernia 448 

CHAPTER  XXVIII. 
Pulmonary  Arteriosclerosis 451 


x  CONTENTS 

SECTION    III. 
DISEASES  OF  THE  PLEURA. 

CHAPTER  XXIX. 

PUBUMTIS I.,,', 

1.  Acute  Fibrinous  Pleuritis l.V.i 

2.  Acute  Serofibrinous  Pkurit is 467 

3.  Acute  Purulent  Pleuritis .".is 

CHAPTER   XXX. 

Special  Forms  of  Pleuritis 531 

1.  Diaphragmatic  Pleurisy .531 

2.  Encysted  Empyema 531 

3.  Actinomycosis  and  Streptothricosis                       533 

4.  Peripleuritis 5:;  I 

5.  Syphilis  of  the  Pleura 535 

6.  Chronic  Pleuritis 535 

CHAPTER  XXXI. 

Hydrothorax 537 

CHAPTER   XXXII. 

Hemorrhagic  Pleural  Fluids 539 

1.  Hemoserothorax 539 

2.  Traumatic  Hemothorax 541 

CHAPTER  XXXIII. 

Chylothorax 546 

CHAPTER  XXXIV. 

Tumors  of  the  Pleura 550 

1.  Benign 550 

2.  Primary  Malignant  Tumors 551 

(a)  Carcinoma 551 

(6)  Sarcoma 555 

3.  Secondary  Malignant  Tumors 556 

CHAPTER   XXXV. 

Echinococcus  Disease  of  the  Pleura 557 

1.  Pleural  Echinococcus 557 

2.  Parapleural  Echinococcus 558 

CHAPTER  XXXVI, 

Pneumothorax    564 


SECTION  I. 
DISEASES  OF  THE  BRONCHI. 


CHAPTER   I. 
BRONCHOSTENOSIS. 

Etiology. — The  causes  may  be  briefly  summarized  and  for  con- 
venience divided  into  those  affecting  the  large  and  medium-sized  and 
the  small  bronchi. 

A.  Stenosis  of  the  Large  and  Medium-sized  Bronchi. — Partial  or 
complete  occlusion  may  be  due  to  the  following: 

1.  Extrabronchial  Causes. — Compression  from  without  may  arise 
from  aortic  aneurysm,  malignant  disease  of  the  lung,  mediastinum, 
or  esophagus,  enlarged  tracheobronchial  lymph  glands,  pericardial 
effusion,  dilatation  of  the  left  auricle,  mediastinal  abscess,  or  echino- 
coccus  disease.  Bronchostenosis  from  dilatation  of  the  left  auricle  is 
probably  more  common  than  is  generally  supposed.  A  slight  degree 
of  stenosis  undetectable  by  ordinary  methods  may  be  recognized  by 
bronchoscopic  examination.  Kahler1  has  reported  13  cases,  in  11  of 
which  the  clinical  diagnosis  was  mitral  stenosis,  1  mitral  insufficiency, 
and  1  aortic  insufficiency.  In  one  case  Schrotter2  noted  narrowing  of 
the  bronchi  from  dislocation  of  the  mediastinum  in  consequence  of 
pneumohydrothorax.  A  discussion  of  these  causes  falls  without  the 
scope  of  this  work. 

2.  Diseases  of  the  Bronchial  Wall. — In  this  group,  benign  and  malig- 
nant tumors,  syphilis,  tuberculosis  and  scleroma  may  be  mentioned 
and  are  described  elsewhere.  The  lesions  of  leprosy,  glanders,  and 
variola  may,  in  rare  instances,  give  rise  to  bronchial  occlusion.  Brindel3 
reported  the  case  of  a  man,  aged  sixty-four  years,  who  was  severely 
wounded  in  the  neck  thirty-four  years  before  by  a  fragment  of  a  shell. 
Thirteen  years  later  a  hard  tumor  appeared  over  the  cicatrix  and 
gradually  increased  to  the  size  of  the  fist,  with  adhesion  to  the  deeper 
parts  and  the  trachea.     Consequent  disturbance  of  respiration  led 

1  Monatsschr.  f.  Ohrenheilk.,  1912,  xlvi,  573. 

2  Klinik  der  Bronchoskopie,  1906,  p.  265. 

3  Atresie  de  la  trachee  et  des  grosses  bronches  par  neoformation  sclereraateuse 
d'origine  traumatique,  Gaz.  hebd.  des  sci.  med.,  26  Fev.,  1905. 

2 


is  DISEASES  OF   THE  BRONCHI 

to  tracheotomy.  Bronchoscopy  showed  diminution  in  the  caliber  of 
the  trachea  and  bronchi.  Histologic  examination  of  the  tumor 
showed  cicatricial  fibrous  tissue. 

3.  Inirabronchial  Causes. — In  this  class  may  be  placed  foreign  bodies 
which  gain  entrance  to  the  air  passages  by  aspiration,  or  arise  from 
within.  They  are  considered  under  a  separate  heading.  Devi1  reports 
sudden  bronchia]  obstruction  from  the  accumulation  of  thick  mucus 
during  an  attack  of  acute  bronchial  catarrh.  Killian2  found  and 
removed,  by  lower  tracheoscopy,  tenacious  secretion  partly  occluding 
the  lower  trachea  and  primary  bronchi  in  a  patient  with  laryngeal 
tuberculosis. 

B.  Stenosis  of  the  Smaller  Bronchi — Owing  to  the  narrow  lumen  of 
the  smaller  passages,  their  proximity  to  the  lung  and  the  small  area 
of  pulmonary  tissue  supplied  by  individual  branches,  occlusion  by 
compression  from  without,  disease  of  the  bronchial  wall  or  foreign 
bodies  fails  to  give  rise  to  striking  clinical  features  referable  to  the 
bronchi  unless  a  large  number  of  the  smaller  passages  are  simulta- 
neously involved.  In  such  conditions  as  widespread  capillary  bronchitis, 
bronchial  asthma  with  spasm  of  the  bronchioles,  bronchitis  fibrosa, 
and  bronchitis  and  bronchiolitis  obliterans,  the  obstruction  to  free 
entrance  and  exit  of  air  may  cause  serious  symptoms.  These  causes 
are  considered  elsewhere. 

Pathology. — Sudden  total  occlusion,  as  by  a  foreign  body,  is  followed 
by  atelectasis  and  reduction  in  size  of  the  part  of  the  lung  supplied 
by  the  occluded  passage  from  absorption  of  air.  Partial  occlusion 
is  more  common,  however,  and  is  followed  by  diminished  air  content 
of  the  affected  pulmonary  territory.  In  early  cases  other  lesions  may 
be  lacking,  but  if  the  occlusion  persists  for  more  than  a  few  days, 
important  changes  occur,  and  for  the  most  part  as  a  result  of  stasis 
of  secretion  and  infection  by  organisms  always  present  and  ready  to 
set  up  inflammatory  processes  in  the  damaged  region  beyond  the 
obstruction.  Retained  mucus  is  transformed  into  mucopurulent 
and  purulent  material.  The  infection  extends  to  the  pulmonary  tissue, 
giving  rise  to  bronchopneumonia,  abscess,  or  gangrene.  Bacterial 
invasion  of  the  bronchial  wall,  the  pressure  of  retained  secretion, 
and  disintegration  of  the  supporting  pulmonary  tissue  lead  to  the 
development  of  bronchiectasis.  Chronic  interstitial  pneumonia  and 
contraction  of  the  pulmonary  tissue  follow  the  more  acute  inflammatory 
processes.  Osier3  speaks  of  the  bronchiectasis  and  pulmonary  suppura- 
tion following  compression  of  a  bronchus  as  aneurysmal  phthisis. 
Extension  to  the  pleura  may  cause  fibrinous,  serofibrinous,  or  purulent 
pleurisy.  Pulmonary  tuberculosis  may  develop.  Its  occurrence  has 
been  specially  noted  in  connection  with  compression  of  the  trachea 


1  Pester  med.  Chir.  Presse,  1884,  xx,  1 15. 
-  Quoted  from  Schrotter,  loc.  cit.,  p.  265. 
3  Practice  of  Medicine,  1905,  p.  856. 


BRONCHOS  TENOSIS  1 9 

or  bronchi  from  aortic  aneurysm.  Of  45  cases  of  aneurysm  of  the 
thoracic  aorta  reported  by  Frankel,1  in  4  there  was  chronic  pulmonary 
inflammation  and  induration  and  in  3  other  cases  (about  7  per  cent.) 
extensive  tuberculosis  with  predominant  infection  of  the  left  lung. 
In  two  of  the  three,  considerable  narrowing  of  the  left  primary 
bronchus  was  noted. 

Symptoms  and  Signs. — The  frequent  coincident  involvement  of  the 
trachea  and  primary  bronchi  in  the  conditions  leading  to  bronchial 
stenosis  makes  it  difficult  or  impossible  in  many  instances  to  draw  any 
sharp  distinction  between  clinical  features  referable  to  one  or  the 
other,  and  the  manifestations  common  to  the  various  causes  of 
tracheobronchial  stenosis  are  first  considered. 

Gerhardt,2  in  his  study  of  syphilitic  tracheal  stenosis,  in  which  the 
important  changes  are  often  just  above  or  at  the  bifurcation,  noted 
three  periods  in  the  clinical  picture,  and  these  are  also  applicable  with 
some  modification  to  tracheobronchial  stenosis  from  other  causes. 
During  the  initial  period  of  a  gradually  increasing  obstruction  there 
may  be  such  irritative  symptoms  as  cough  with  or  without  expectoration, 
a  substernal  tickling  or  uncomfortable  sensation,  weakening  of  the 
voice,  and  slight  dyspnea  on  exertion.  As  the  lumen  of  the  involved 
passage  diminishes,  the  first  passes  insensibly  into  the  second  stage, 
in  which  there  is  persistent  dyspnea  with  the  patient  at  rest,  and  this 
in  turn  into  the  third  and  final  stage  of  suffocation  and  death.  The 
different  periods  are  often  not  clearly  recognizable,  and  transient 
suffocative  attacks,  with  cyanosis,  severe  dyspnea,  and  even  uncon- 
sciousness for  a  time  may  appear  early  and  recur  at  intervals  throughout 
the  disturbance.  They  may  be  due  to  catarrhal  swelling  of  the  mucous 
membrane  about  the  site  of  a  partial  obstruction,  to  occlusion  by 
secretion,  or  to  acute  cardiac  dilatation.  The  strain  upon  the  heart 
as  a  consequence  of  tracheobronchial  obstruction  is  probably  largely 
due  to  increase  of  pressure  in  the  pulmonary  circuit  during  forced 
expiration. 

Hoarseness  may  be  due  to  coincident  disease  of  the  larynx  or  recur- 
rent laryngeal  paralysis,  but  weakness  of  the  voice  may  be  observed 
quite  independent  of  a  disturbance  of  the  larynx  and  may  be  ascribed 
to  diminished  volume  of  the  air  current  in  consequence  of  the  trouble 
below. 

The  dyspnea  of  tracheobronchial  obstruction  is  both  inspiratory 
and  expiratory.  Predominant  expiratory  dyspnea  is  occasionally 
observed,  and  may  be  ascribed  to  the  narrowing  of  the  caliber  of  the 
trachea  and  bronchi  and  greater  obstruction  to  the  passage  of  air 
through  an  already  partially  occluded  lumen  during  this  phase  of 
respiration.  The  head  may  be  held  forward  with  the  chin  approaching 
the  chest,  for  the  purpose  of  relaxing  and  widening  the  trachea.    Imnio- 

1  Spez.  path.  u.  Ther.  d.  Lungenkrankheiten,  1904,  p.  65. 

2  Deut.  Arch.  f.  klin.  Med.,  1866-67,  ii,  538. 


20  DISEASES  OF  THE  BRONCHI 

bility  of  the  larynx  during  respiration  may  be  noted.  These  features 
may  be  contrasted  with  the  predominant  inspiratory  dyspnea,  ten- 
dency to  hold  the  head  backward,  and  greater  amplitude  of  laryngeal 
excursion  with  .laryngeal  stenosis.  The  use  of  the  accessory  muscles 
of  respiration,  the  inspiratory  depression  of  the  tissues  at  the  root  of 
the  neck,  the  intercostal  spaces,  the  epigastrium,  and  the  lower  parts 
of  the  chest  in  the  region  of  the  diaphragmatic  attachment  may  also 
be  noted.  Inspiratory  and  expiratory  or  predominantly  expiratory 
stridor  may  be  heard.  It  is  spoken  of  as  "cornage"  by  the  French, 
and  is  due  to  the  passage  of  air  through  an  obstructed  tube. 

On  examination  of  the  lungs,  little  or  nothing  of  significance  may 
be  found  early  in  the  course  of  tracheobronchial  obstruction,  and  before 
secondary  inflammatory  processes  have  arisen  below  the  point  of 
obstruction.  The  stridor  ma)'  be  of  maximum  intensity  to  one  or  the 
other  side  of  the  median  line,  as  an  indication  of  its  point  of  origin; 
but  it  may  be  conducted  along  the  trachea  to  the  neck  and  heard  best 
in  this  region  when  the  site  of  obstruction  is  below.  A  considerable 
degree  of  obstruction  may  lead  to  inflation  of  the  lung,  hyper- 
resonance,  relative  immobility,  and  abnormally  low  position  of  the 
pulmonary  margin  and  other  signs  of  emphysema. 

With  unilateral  bronchostenosis  the  symptoms  are  the  same,  but  less 
severe  than  with  tracheobronchial  obstruction.  Complete  sudden 
closure  of  a  primary  bronchus  is  followed  by  severe  dyspnea  and  suffo- 
cative symptoms,  which  usually  subside  after  a  short  time,  and  seldom 
terminate  fatally  unless  complicated  by  other  disturbances  in  the 
respiratory  or  circulatory  system.  Following  the  initial  disturbance  of 
sudden  occlusion,  or  in  the  course  of  a  gradually  increasing  partial 
obstruction,  troublesome  dyspnea  may  be  present  only  on  exertion. 
On  examination,  diminished  respiratory  excursion,  resonance  on 
percussion,  and  weakened  breath  sounds,  voice,  whisper,  and  tactile 
fremitus  are  found  over  the  parts  of  the  lung  supplied  by  the  occluded 
bronchus.  Measurement  may  show  some  narrowing  of  the  affected 
side.  Stridor  may  be  heard  over  the  site  of  the  obstruction.  Signs 
of  compensatory  emphysema  can  be  demonstrated  over  the  unaffected 
lung. 

Clinical  manifestations  arising  in  consequence  of  obstruction  of 
individual  bronchi  become  less  striking  and  less  typical,  the  more 
gradual  the  obstruction  and  the  smaller  the  occluded  passage.  It  not 
infrequently  happens  that  bronchostenosis  arising  from  disease  of  the 
bronchial  wrall  or  foreign  bodies  is  masked  by  manifestations  referable 
to  secondary  infection  of  the  lung,  or  that  bronchial  obstruction  due 
to  compression  from  without  is  an  inconspicuous  and  unheeded  incident 
in  the  course  of  serious  intrathoracic  disease,  the  clinical  features  of 
which  dominate  the  picture. 

Diagnosis. — The  differentiation  between  bronchostenosis  arising 
from  compression  and  that  due  to  endobronchial  causes  is  at  times 
difficult  or  impossible.     The  extrabronchial  causes  comprise,  for  the 


BRONCHOSTENOSIS  21 

most  part,  disease  which  develops  in  or  about  the  mediastinum  or 
invades  this  region,  as  in  the  case  of  malignant  disease  by  metastasis. 
They  may  give  indication  of  their  presence  by  dulness  in  the  supra- 
cardiac  region  or  over  the  vertebra?  between  the  third  and  the  ninth 
dorsal  spines,  and  such  signs  of  pressure  upon  other  organs  as  dys- 
phagia, inequality  of  the  pupils  or  the  pulses,  variation  in  the  blood- 
pressure  in  the  two  arms,  "tracheal  tug,"  recurrent  laryngeal  paralysis, 
engorgement  of  the  vessels  of  the  head  and  neck  or  one  arm,  and  dilated 
superficial  thoracic  veins.  A  history  of  syphilis,  attacks  of  pain  like 
angina  pectoris,  pulsation  of  the  dull  area,  systolic  thrill  and  murmur, 
diastolic  shock,  and  aortic  regurgitation  speak  for  aneurysm.  Cachexia 
and  enlarged  cervical  or  axillary  glands  suggest  malignant  disease. 
Mediastinal  involvement  in  a  child  with  tuberculosis  is  likely  to  be 
due  to  enlarged  and  tuberculous  glands.  Examination  with  the  .r-rays 
is  important,  and  may  lead  to  the  detection  of  extrabronchial  disease, 
of  which  there  is  no  indication  on  physical  examination. 

In  the  absence  of  indications,  on  physical  and  radioscopic  examina- 
tion, of  an  extrabronchial  cause,  foreign  body  or  disease  of  the  bronchial 
wall  may  be  suspected.  If  there  is  a  definite  history  of  aspiration  of 
a  foreign  body,  followed  by  pulmonary  symptoms  and  signs  of  unilateral 
bronchostenosis,  the  diagnosis  is  easily  made,  but  it  is  important  to 
remember,  as  is  noted  in  the  section  on  aspirated  foreign  bodies,  that 
there  may  be  nothing  in  the  history  or  physical  examination  to  indi- 
cate such  a  cause.  Here  also  radioscopic  examination  may  be  helpful, 
but  negative  a;-rays  do  not  exclude  a  foreign  body. 

Bronchostenosis  from  syphilis  may  be  suspected  in  a  syphilitic 
subject  after  the  exclusion  of  other  causes.  Scleroma  and  tuberculosis 
are  uncommon,  and  there  are  usually  other  indications  pointing  to 
the  diagnosis.  Primary  malignant  disease  of  the  bronchi  is  the  most 
difficult  of  diagnosis. 

Important  advances  in  methods  of  investigation  have  made  it 
possible  in  many  instances  to  resolve  the  difficulty  of  establishing  the 
cause  of  bronchostenosis  in  doubtful  cases.  Laryngoscopy,  tracheo- 
scopy, and  bronchoscopy,  with  suitable  instruments  in  skilful  hands, 
now  permit  earlier  and  more  accurate  diagnosis,  and  more  especially 
in  the  case  of  foreign  bodies  and  syphilis  the  institution  of  earlier  and 
more  successful  treatment.  A  discussion  of  bronchoscopy  will  be  found 
in  the  section  on  Foreign  Bodies. 

Prognosis  and  Treatment. — The  prognosis  depends  on  the  cause  of 
the  occlusion.  The  outlook  is  grave  in  any  case  in  which  the  obstruc- 
tion cannot  be  removed.  It  is  most  unfavorable  with  malignant  disease, 
only  little  better  in  aneurysm,  and  adds  to  the  seriousness  of  tuber- 
culous glands,  pericardial  effusion,  dilated  left  auricle,  and  mediastinal 
abscess  or  echinococcus  disease,  the  dangers  of  mechanical  hindrance 
to  respiration,  cardiac  strain,  and  pulmonary  infection  beyond  the 
obstruction.  If  discovered  early,  syphilis  offers  considerable  hope 
of  relief.    The  prospect  with  foreign  bodies  grows  increasingly  bright 


22  DISEASES  OF  THE  BRONCHI 

with  advances  in  bronchoscopic  removal,  and  even  the  chronic  eases 

should  not  be  regarded  as  hopeless.    Further  discussion  of  prognosis 
and  treatment  will  be  found  in  the  separate  sections. 


1.  TUMORS  OF  THE  BRONCHI. 

Benign  Tumors. — These  occur  only  in  very  rare  instances.  In 
Rokitansky's1  case  a  submucous  lipoma  almost  filled  the  lumen  of  the 
left  primary  bronchus.  Seigert2  at  autopsy  found  a  papilloma  at  the 
bifurcation  of  the  trachea  apparently  filling  the  trachea  and  projecting 
into  the  right  bronchus.  Spiess3  found  a  polyp,  4  cm.  long  and  1.5  cm. 
thick,  taking  its  origin  from  the  right  bronchus  just  below  the  bifur- 
cation. The  right  bronchus  was  completely  and  the  left  partially 
occluded.  There  were  cough,  severe  dyspnea,  and  attacks  of  suffo- 
cation. The  tumor  was  successfully  removed  by  lower  bronchoscopy. 
E/ichondromas  have  been  observed.  Tumors  containing  cartilage  may 
occur  as  flat,  rounded,  or  nodular  circumscribed  growths,  taking  their 
origin  from  the  larger  or  smaller  bronchi.  It  is  difficult  to  differentiate 
simple  hyperplasia  or  enchondrosis  and  true  enchondroma.  A  bean- 
shaped  cartilaginous  tumor  occluding  the  lumen  of  a  bronchus  to  the 
right  middle  lobe  and  leading  to  bronchial  dilatation  is  described  by 
Siegert.4  Eicken5  removed  from  the  left  primary  bronchus  by  means 
of  bronchoscopy  a  polypous  mass  containing  islands  of  cartilage.  In 
Blecher's6  case  there  was  found  at  autopsy  a  hard,  spherical  tumor, 
(ossified  enchondrosis  of  a  bronchial  cartilage)  the  size  of  a  hazelnut, 
in  the  left  primary  bronchus,  beyond  which  the  bronchi  were  dilated. 
Chiari7  reported  an  intrabronchial  tumor  of  a  complicated  structure 
(lipoma,  chondroma,  and  adenoma). 

Malignant  Tumors. — The  malignant  tumors  of  the  bronchi  may 
spring  from  the  primary  bronchi  or  their  larger  or  smaller  divisions, 
and  are  usually  cylindrical-celled  carcinoma,  less  commonly  flat-celled 
carcinoma.  Extension  by  way  of  the  lymph  channels  or  direct  con- 
tinuity soon  leads  to  malignant  disease  of  the  neighboring  or  more 
remote  parts  of  the  lung  and  peribronchial  or  other  lymph  glands. 
When  the  growth  develops  from  the  wall  of  the  primary  bronchus 
or  one  of  its  larger  branches  it  soon  leads  to  occlusion  of  the  bronchial 
lumen,  with  bronchitis,  bronchiectasis,  abscess  formation,  and  broncho- 
pneumonia and  interstitial  pneumonia  in  the  affected  region.    Although 

1  Lehrb.  d.  path.  Anat.,  1861,  Band  iii. 

2  Virchow's  Arch.,  Band  cxxix,  p.  413. 

3  Munch,  med.  Woch.,  4  Okt.,  1910. 

4  Virchow's  Arch.,  1892,  Band  cxxix. 

5  Verhandl.  d.  Vereines  silddeutsch.,  Laryngolog.,  1907. 

6  Ueber  die  klinische  Bedeutung  d.  Bronchialekchondrosen,  Mitt.  a.  d.  Grenzgeb. 
d.  Med.  u.  Chir.,  1910,  xxi,  837. 

7  Prager  med.  Woch  ,  1883,  viii. 


SYPHILIS  OF  THE  TRACHEA  AND'  BRONCHI  23 

the  question  cannot  yet  be  regarded  as  settled,  it  is  probable  that  car- 
cinoma of  the  lung  almost  invariably  arises  from  the  bronchi.  The 
clinical  features  are  predominantly  pulmonary,  and  malignant  tumors 
of  the  bronchi  are  therefore  discussed  under  Tumors  of  the  Lung. 


2.  SYPHILIS    OF    THE    TRACHEA   AND   BRONCHI. 

The  initial  sore  of  syphilis  has  not  been  observed  in  the  trachea 
or  bronchi.  Such  secondary  lesions  as  catarrhal  inflammation,  hyper- 
emic  spots,  and  mucous  patches  have  been  noted  in  rare  instances, 
but  are  of  little  clinical  importance.  Tertiary  manifestations  are 
found  with  diminishing  frequency  from  above  downward,  occurring 
commonly  in  the  uppermost  parts  of  the  tract,  less  often  between 
pharynx  and  trachea,  and  only  rarely  in  the  trachea  and  bronchi. 

Munk's1  case  seems  to  have  been  the  first  in  which  disease  of  the 
trachea  and  bronchi  was  ascribed  to  syphilis.  In  1867,  Gerhardt2 
reported  5  cases  and  summarized  the  clinical  features.  In  1878 
Vierling3  collected  46  eases,  to  which,  in  1903,  Conner4  added  82. 
Conner's  article  is  the  most  complete  and  careful  study  in  the  litera- 
ture. Recently  the  number  of  reported  cases  has  rapidly  increased, 
owing  to  the  greater  frequency  of  diagnosis  by  means  of  bronchoscopy. 
Schrotter5  was  able  to  report  in  1896  that  13  cases  of  tracheobronchial 
syphilis  had  come  under  his  observation,  from  which  the  conclusion 
may  be  drawn  that  careful  bronchoscopic  investigation  discloses  more 
cases  than  would  otherwise  be  found.  Tracheal  ulceration  ascribed 
to  syphilis  was  found  in  only  2  cases  (Nos.  29  and  1196)  among 
3000  autopsies  at  the  Massachusetts  General  Hospital. 

Tracheobronchial  manifestations  may  follow  acquired  or  inherited 
syphilis,  a  variable  interval  elapsing  between  infection  and  the  onset  of 
symptoms.  Of  31  cases  of  acquired  syphilis  in  Conner's6  series  in 
which  the  interval  was  noted  it  averaged  ten  years,  the  extremes  being 
nine  months  and  forty-two  years.  In  10  cases  of  inherited  syphilis 
the  average  age  was  ten  years,  the  two  oldest  cases  being  nineteen 
and  twenty  years. 

The  upper  or  lower  third  of  the  trachea  is  most  frequently  involved, 
the  region  just  above  the  bifurcation  being  a  point  of  election.  Com- 
bined lesions  of  the  lower  end  of  the  trachea  and  the  bronchi  are  com- 
mon. In  some  cases  one  or  both  bronchi  alone  are  involved.  Bronchial 
branches  of  the  third  or  fourth  order  are  rarely  if  ever  invaded.  The 
frequency  of  syphilitic  manifestations  in  the  region  of  the  tracheal 
bifurcation  and  the  main  bronchi  may  be  ascribed  to  local  irritation 

1  London  Medical  Gazette,  1841,  p.  20. 

2  Deut.  Arch.  f.  klin.  Med.,  1867,  ii,  535.  3  Ibid.,  vol.  xxi,  p.  325. 
4  Amer.  Jour.  Med.  Sci.,  1903,  N.  S.,  cxxvi. 

6  Klinik  der  Bronchoskopie,  1906,  p.  342.  6  Loc.  cit. 


24  DISEASES  OF  THE  BRONCHI 

"I  the  tissue  by  dust  particles  in  consequence  of  the  division  of  the 
air  current. 

Pathology. — Three  principal  pathologic  lesions,  representing  the 
evolution  of  the  syphilitic  process,  may  be  recognized  singly  or  com- 
bined in  the  same  or  different  cases.  (1)  Gwnmata  occur  as  circum- 
scribed or  diffuse,  single  or  multiple,  large  or  small  reddish  masses, 
projecting  into  and  encroaching  on  the  lumen  of  the  trachea  or  bronchi. 
They  may  be  rounded  or  irregular  and  hard  or  soft.  In  some  instances, 
fibrinous  or  purulent  exudate  or  ulceration  is  seen  on  the  surface. 
(2)  Ulcers  may  be  single  or  multiple,  discrete  or  confluent,  large  or 
small  and  superficial  or  deep,  irregular  or  circular  in  outline,  and  with 
a  thick  or  thin  and  at  times  undermined  margin.  The  loss  of  substance 
may  be  confined  to  the  mucosa  or  submucosa,  or  include  the  fibro- 
cartilaginous layer,  with  erosion  and  destruction  of  cartilage,  fragments 
of  which  may  be  expectorated.  Cicatrization  may  or  may  not  accom- 
pany the  destructive  changes.  Perforation  of  the  trachea  or  bronchi 
and  extension  to  neighboring  tissues  may  occur.  Mediastinal  abscess 
and  perforation  of  the  esophagus  have  been  observed.  The  opening 
of  a  bloodvessel  may  be  followed  by  fatal  hemorrhage.  Circumscribed 
or  diffuse  (3)  scars  develop  as  a  result  of  the  syphilitic  process.  Endo- 
tracheal or  endobronchial  increase  of  connective  tissue  leads  to  the 
production  of  cicatrices  of  variable  shape  and  extent,  always  tending 
to  narrow  and  at  times  even  obliterating  the  lumen  of  the  affected 
passage.  Band-like,  annular  or  membranous  strictures  may  be  found. 
Gerhardt1  likened  the  resulting  appearance  of  the  trachea  to  that  of 
a  rope-ladder.  Fibrous  peritracheitis  or  peribronchitis  may  involve 
adjacent  structures,  especially  the  recurrent  laryngeal  nerves.  Asso- 
ciated enlargement  of  the  tracheobronchial  glands  may  cause  com- 
pression stenosis.  Tracheal  or  bronchial  dilatation  may  be  found 
above  and  below  an  obstruction. 

Old  or  recent  syphilis  of  the  mouth,  nose,  pharynx,  or  larynx  may 
be  present.  Bronchiectasis  below  the  obstruction  is  not  uncommon, 
and  may  be  ascribed  to  the  stenosis,  weakening  of  the  bronchial  wall 
and  the  adjoining  pulmonary  tissue  from  syphilis  or  other  disease. 
Lobar  or  bronchopneumonia  may  complicate  the  process.  Coexistent 
pulmonary  tuberculosis  is  occasionally  observed.  Emphysema  is  not 
infrequent. 

Symptoms  and  Signs. — An  initial  stage  of  irritation,  followed  in 
turn  by  permanent  stenosis,  and  finally  by  suffocative  attacks,  as 
noted  by  Gerhardt,2  may  be  recognized  in  many  cases.  Cough  is 
commonly  the  earliest  symptom  and  is  at  first  dry,  but  later  accom- 
panied by  mucoid,  mucopurulent  or  purulent,  and  occasionally  blood- 
streaked  sputum.  Elastic  tissue  may  be  found  in  the  sputum.  Hem- 
optysis, when  it  occurs,  is  a  prominent  symptom  in  about  half  of  the 

1  Loo.  cit.  2  Loc.  cit. 


SYPHILIS  OF  THE  TRACHEA  AND  BRONCHI  25 

cases.  Of  16  cases  in  which  it  was  noted  it  was  of  minor  importance 
in  9  0  to 9)  and  fatal  in  7  (10  to  16). 

In  3  (10,  n,  13)  of  the  7  fatal  cases  the  bleeding  was  preceded  by 
hemorrhage.  An  autopsy  was  performed  on  6  and  disclosed  ulceration 
of  the  trachea  and  bronchi  with  perforation  of  the  pulmonary  artery 
in  3  (14  to  16)  and  the  aorta  (u),  branches  of  the  bronchial  artery 
(12),  and  the  superior  vena  cava  (13)  in  1  each.  Hemorrhage  may  be 
the  first  striking  symptom,  as  in  1  of  the  Massachusetts  General 
Hospital  cases  reported  by  Gannett.17  The  patient,  a  man,  aged 
thirty-seven  years,  had  coughed  without  expectoration  for  three  years. 
He  had  an  abundant  hemoptysis  three  days  before  entrance.  Death 
occurred  two  days  after  admission  from  a  recurrence  of  the  bleeding 
and  at  autopsy  (No.  1196)  it  was  found  that  a  large  branch  of  the 
pulmonary  artery  had  ruptured  into  the  right  primary  bronchus 
through  a  cicatrix  involving  the  wall  of  the  bronchus  and  the  artery. 
Other  cicatrices  were  found  in  the  trachea  and  the  left  primary  bron- 
chus. Interstitial  orchitis  with  the  findings  in  the  trachea  and  bronchi 
suggested  syphilis  as  a  cause. 

Symptoms  of  tracheobronchial  stenosis  are  seldom  absent.  Per- 
sistent or  paroxysmal  dyspnea  is  the  most  constant  and  conspicuous 
manifestation,  and  may  be  ascribed  to  the  obstruction  to  respiration 
and  consequent  cardiac  insufficiency. 

Suffocative  attacks  may  follow  exertion  or  occur  at  night.  They 
are  probably  due  to  acute  failure  of  an  already  overtaxed  heart. 
During  the  paroxysm,  orthopnea,  cyanosis,  inspiratory  or  both  inspi- 
ratory and  expiratory  dyspnea  and  stridor;  relative  immobility  of  the 
larynx;  inspiratory  retraction  of  the  tissues  at  the  root  of  the  neck,  the 
lower  intercostal  spaces,  and  the  epigastrium;  diminished  respiratory 
motion  and  feeble  vesicular  murmur,  weak  pulse,  and  even  unconscious- 
ness may  be  noted.  On  auscultation  the  stridor  may  be  of  maximum 
intensity  over  the  site  of  the  obstruction.  In  Prengrueber's18  case, 
a  suffocative  attack,  after  running  up  stairs,  was  the  first  symptom. 

1  Hanzel,  Wein.  klin.  Woch.,  189S,  xi,  955. 

2  Parrain,  These,  Bordeaux,  1894,  No.  89.     Quoted  from  Conner. 

3  Chiari,  Schrotter's  case,  Monatschr.  f.  Ohrenh.,  1881,  xv,  196. 

4  Lancereux,  Ann.  des  mal.  d'Or.,  1882,  p.  117. 

6  Gairdner,  Glasgow  Med.  Jour.,  1890,  xxxiii,  463. 

6  Silcock,  Trans.  Path.  Soc.,  London,  1886,  xxxvii,  115. 

7  Wright,  New  York  Med.  Jour.,  1891,  liii,  672. 

8  Wright,  ibid. 

9  Norton,  Trans.  Path.  Soc.,  London,  1872,  xxiii,  44. 

10  Sokolowsky,  Berl.  klin.  Woch.,  1889,  xxvi,  209. 

11  Barnays,  St.  Louis  Med.  and  Surg.  Jour.,  1880,  xxxix,  250. 

12  Watson,  New  York  Jour,  of  Med.,  1843,  i,  57. 

13  Turner,  Trans.  Path.  Soc,  London,  1886,  xxxvii,  117. 

14  Gerhardt,  Deut.  Arch.  f.  klin.  Med.,  1867,  ii,  541. 

16  Kelly,  Trans.  Path.  Soc,  London,  January  2,  1872,  p.  45. 

16  Gannett,  Boston  Med.  and  Surg.  Jour.,  July  21,  1904. 

17  Loc  cit. 

18  Algerie  Medicale,  1870:  also  Rey.  Syphilis  tracheale,  Paris,  1874,  quoted  from 
Conner,  loc  cit. 


26  DISEASES  OF  THE  BRONCHI 

and  was  follow  til  by  many  similar  attacks,  during  which  the  patient 
was  for  many  hours  unconscious,  with  barely  perceptible  pulse,  while 
in  the  intervals  she  was  quite  well.  In  11  of  the  cases  collected  by 
Conner1  the  patient  died  in  a  suffocative  attack.  In  Wadsack's2 
2  rases  a  sudden  and  fatal  attack  of  suffocation  terminated  a  period 
of  comparative  health.  Pain  of  a  dull  character  and  usually  referred 
to  the  substernal  region  is  at  times  observed.  Dysphagia  and  aphonia 
may  also  be  noted. 

Unilateral  bronchostenosis  may  be  indicated  by  diminished  respira- 
tory motion,  breathing,  voice,  whisper,  and  tactile  fremitus  on  the 
affected  side. 

Fig.  1 


Syphilitic  narrowing  of  the  trachea,  beginning  2  cm.  above  the  bifurcation.      Left 
bronchus  almost  closed.     Right  bronchus  much  narrowed.     (Wadsack.) 

Diagnosis. — Tracheobronchial  syphilis  may  be  suspected  when  there 
is  a  history  of  the  disease  and  such  symptoms  as  cough,  dyspnea, 
bloody  sputum,  or  frank  hemoptysis  in  the  absence  of  other  obvious 
cause.  .Manifestation  of  late  syphilis  elsewhere,  especially  in  the  upper 
parts  of  the  respiratory  tract,  failure  to  react  to  tuberculin,  a  positive 
Wassermann  test,  and  symptoms  of  tracheobronchial  stenosis  are 
important  additional  evidence.     Foreign  bodies  in  the  air  passages, 

1  Loc.  cit. 

2  Zwei  plotzliche  Todesfalle  infolge  syphilitischer  Bronchostenose,  Charite  Annalen, 
1905,   xxix,   211. 


TUBERCULOSIS  OF  THE  BRONCHI  27 

tumors  developing  from  the  wall,  and  compression  from  without  are 
most  likely  to  offer  difficulty  of  differentiation.  Examination  with  the 
x-ray  will  be  of  assistance  in  reaching  a  decision.  Direct  inspection 
by  tracheoscopy  or  bronchoscopy  may  demonstrate  ulceration  and 
scarring  of  the  trachea  and  bronchi.  Such  lesions  are  seldom  due  to 
other  causes  than  syphilis,  but  neither  the  macroscopic  nor  the  micro- 
scopic appearances  can  be  regarded  as  establishing  the  diagnosis. 
Syphilis  and  tuberculosis  cannot  thus  be  distinguished,  and  only  the 
demonstration  of  the  spirochseta  of  syphilis  is  conclusive.  In  doubtful 
cases,  therefore,  the  investigation  of  a  small  piece  of  excised  tissue  will 
be  helpful. 

Prognosis. — Thus  far  the  mortality  has  been  high.  In  Vierling's1 
46  cases  death  occurred  in  39.  In  Conner's2  82  cases  there  were  58 
deaths,  giving  a  mortality  of  76  per  cent,  in  the  two  series.  Pneu- 
monia, a  suffocative  attack,  hemorrhage  from  perforation  of  a  large 
bloodvessel,  exhaustion,  or  cardiac  failure  are  the  most  common 
causes.  The  possibility  of  diagnosis  by  tracheoscopy  and  bronchos- 
copy during  the  early  gummatous  or  ulcerative  stage  of  the  infection, 
and  while  treatment  may  still  be  effective,  may  be  expected  to  favor- 
ably influence  the  chances  of  recovery.  Tracheobronchial  stenosis 
from  firm,  unyielding,  and  irremediable  cicatrices  is  very  unfavorable. 
The  outlook  is  less  hopeful  the  deeper  down  in  the  tract  the  syphilitic 
process  occurs.  The  prognosis  is  worse  with  bronchial  than  with 
tracheal  syphilis. 

Treatment.— Chief  reliance  should  be  placed  on  salvarsan  and 
mercury.  The  earlier  the  treatment  is  begun  the  better  the  chances 
of  success.  In  3  cases  reported  by  Kehler,3  in  which  the  diagnosis 
was  made  by  bronchoscopy  before  the  disease  had  advanced  beyond 
the  stage  of  gummata  or  superficial  ulceration,  cure  was  accom- 
plished with  little  resulting  stenosis.  By  bronchoscopic  examination 
Halle4  saw  gummata  of  the  trachea  disappear  in  fourteen  days  after 
the  administration  of  0.6  gram  of  salvarsan.  Mechanical  dilatation 
of  a  stricture  has  occasionally  given  relief,  but  is  not  unattended  with 
danger.  In  the  case  reported  by  Seifert,5  cicatricial  stenosis  of  the 
trachea  and  left  main  bronchus  was  almost  completely  relieved  after 
ten  weeks  of  almost  daily  dilatation  of  the  obstruction. 


3.  TUBERCULOSIS  OF  THE  BRONCHI. 

The  trachea  and  bronchi  are  occasionally  the  site  of  tuberculous 
invasion  as  a  result  of  secondary  infection  from  the  lungs  or  bronchial 
glands.     Single  or  multiple  ulcers  with  consecutive  contraction  and 

1  Loc.  cit.  2  Loc.  cit. 

"3  Wiener  klin.  Woch.,  1909,  li,  2902  and  2963. 
4  Berl.  klin.  Woch.,  January  2,  1911.. 
6  Munch,  med.  Woch.,  1895,  xlii,  719. 


28  DISEASES  OF  THE  BRONCHI 

stenosis  of  the  trachea  or  bronchi  may  result.  The  infrequency  of  the 
disease  in  the  trachea  and  bronchi  may  be  ascribed  to  the  rapidity 
with  which  infected  material  is  expelled  by  cough,  the  absence  of  folds 
and  depressions  in  which  such  material  may  lodge,  the  protection 
which  a  thin  layer  of  mucus  affords  to  the  walls  of  the  air  passages, 
and  the  expulsion  of  small  particles  by  ciliary  motion.  With  rare 
exceptions  only,  tracheobronchial  tuberculosis  is  an  inconspicuous 
incident  in  the  course  of  graver  pulmonary  manifestations  of  the 
disease. 

Primary  tuberculosis  of  the  trachea  or  bronchi  lias  been  established 
in  only  a  few  cases.  In  1901  Gidionsen1  reported  the  case  of  a  woman, 
aged  forty-one  years,  in  whom  death  followed  hemoptysis.  At  autopsy 
dilated  and  varicose  veins  were  found  in  the  trachea,  and  on  the  poste- 
rior wall  just  above  the  bifurcation  an  elongated  ulcer  about  the  size 
of  a  pfennig  piece.  The  lungs  were  free  from  tuberculosis.  Although 
the  ulceration  was  ascribed  to  tuberculosis  and  the  microscopic  sections 
submitted  to  Weigert,  yet  syphilis  cannot  be  regarded  as  adequately 
excluded  in  view  of  the  wrell-known  difficulty  of  differentiating  the 
two  conditions  from  the  histologic  picture.  In  1904  Hedinger2 
reported  the  case  of  a  woman,  aged  twenty-nine  years,  whose  clinical 
history  could  not  be  obtained,  but  in  whom  at  autopsy  multiple 
ulcers  of  the  lower  part  of  the  trachea  and  the  bronchi  were  found. 
The  lumina  of  both  primary  bronchi  were  much  narrowed.  The 
histologic  picture  was  typical  of  tuberculosis,  but  no  tubercle  bacilli 
could  be  found.  No  other  evidence  of  tuberculosis  was  found  in  the 
body.  In  this  case  also  the  proof  of  the  tuberculous  nature  of  the 
disease  is  incomplete.  In  Hansemann's3  patient,  a  woman,  aged 
seventy-three  years,  thorough  search  of  the  body  failed  to  reveal 
tuberculous  lesions  elsewhere  than  in  the  trachea,  where  ulceration 
extended  above  to  the  larynx  and  below  to  beyond  the  bifurcation. 
The  tuberculous  nature  of  the  ulceration  was  first  recognized  micro- 
scopically by  the  finding  of  bacilli.  Schmorl4  reported  2  cases  of  primary 
tuberculosis  of  the  trachea  and  large  bronchi.  In  the  first,  a  boy, 
aged  eighteen  years,  who  died  of  typhoid,  an  unulcerated  tubercle 
half  the  size  of  a  pin's  head  was  found  in  the  left  principal  bronchus. 
In  the  second,  a  child,  aged  eight  years,  a  group  of  three  tubercles 
larger  than  millet-seeds  wTas  found  in  the  trachea. 


4.  SCLEROMA. 

This  is  the  same  disturbance  which  is  spoken  of  in  the  nose  as 
rhinoscleroma.     It  is  probably  identical  with  Gerhardt's5  chorditis 

1  Munch,  med.  Woch.,  1901,  No.  42. 

2  Verhandl.  d.  path.  Gesellsch.,  1904,  vii,  83. 

3  Ibid.,  p.  88.  4  Ibid.,  p.  88. 
6Deut.  Arch.  f.  klin.  Med.,  xi,  583. 


ASPIRATED  FOREIGN  BODIES  29 

vocalis  hypertrophica  inferior  in  the  larynx  and  Stoerk's1  chronic 
blennorrhea  of  the  nose,  larynx,  and  trachea.  It  is  seldom  observed 
in  this  country,  and  is  apparently  most  common  in  Europe  among 
the  poorer  classes  in  and  about  Cracow,  where  Pieniazek  has  had  the 
opportunity  of  studying  many  cases.  In  1905  his  assistant,  Nowotny2 
reported  on  42  cases  in  which  tracheobronchial  stenosis  was  due  to 
scleroma.  The  cause  is  unknown.  The  disease  usually  begins  in  the 
nose  and  thence  slowly  extends  into  the  nasopharynx,  larynx,  and 
trachea.  In  rare  instances  the  trachea  is  primarily  involved,  as  in 
one  of  Nowotny's  cases.  Extension  into  the  primary  and  even  the 
secondary  bronchi  is  occasionally  observed.  The  lesions  first  appear 
as  reddish  infiltrations,  resembling  granulation  tissue,  involving  parts 
or  the  whole  of  the  tract,  with  catarrh  of  the  surface,  the  formation 
of  dried  masses  of  secretion,  and  subsequent  transformation  into  con- 
nective tissue,  with  little  tendency  to  the  production  of  ulceration. 
Great  thickening  and  deformity  of  the  wall  and  narrowing  of  the  lumen 
may  result.  According  to  Nowotny  the  thickening  and  flattening  of 
the  carina  trachea?  is  typical  and  unlike  that  seen  in  any  other  disease. 
Stenosis  of  a  bronchus  may  be  followed  by  the  development  of  bron- 
chiectasis beyond  the  point  of  obstruction.  The  symptoms  are  such 
as  are  seen  in  tracheobronchial  stenosis  from  other  causes.  The  dis- 
ease may  last  for  many  years  and  is  incurable,  but  in  rare  instances 
spontaneous  healing  takes  place.  Treatment  consists  in  the  removal 
of  infiltrations  by  curettage,  the  rupture  of  membranous  bands,  and 
the  dilatation  of  strictures  with  the  assistance  of  tracheoscopy  or 
bronchoscopy. 

5.  ASPIRATED   FOREIGN   BODIES. 

A  number  of  valuable  monographs  have  appeared  dealing  with  the 
aspiration  of  foreign  bodies  into  the  air  passages.  In  1854  Gross3 
collected  nearly  50  cases.  In  1893  Preobraschensky4  analyzed  763 
cases,  to  which,  in  1902,  Pohl5  added  312.  These  publications  deal 
with  the  aspiration  of  foreign  bodies  into  all  parts  of  the  air  passages, 
while  their  lodgement  in  the  bronchi  only  concerns  us  here.  Recently 
interest  in  this  subject  has  centred  principally  in  the  rapid  advances 
made  in  diagnosis  and  treatment  through  the  use  of  the  bronchoscope. 
In  1907  Gottstein6  collected  137  cases  reported  to  April  1,  1906,  in 
which  the  bronchoscope  had  been  used.     His  discussion  is  full  and 

1  Klinik  d.  Krankh.  d.  Kehlkopfes,  etc.,  Stuttgart,  1880,  p.  161. 

2  Arch.  f.  Laryngolog.  u.  Rhinolog.,  1905,  xvii. 

3  A  Practical  Treatise  on  Foreign  Bodies  in  the  Air  Passages,  Philadelphia,  Blanchard 
&  Lea,  1854. 

4  Ueber  Fremdkorper  in  den  Athmungswegen,  Wiener  Klinik,  1893,  xix. 

5  Ueber  Fremdkorper  im  Kehlkopf,  in  der  Luftrohre  und  in  den  Bronchien,  Inaug. 
Diss.,  Breslau,  1902. 

6  Ueber  die  Diagnose  und  Therapie  der  Fremdkorper  in  den  unteren  Luftwegen  mit 
besonderer  Berucksichtigung  der  Bronchoskopie  und  Radioskopie,  Mitt.  a.  d.  Grenzg. 
d.  Med.  u.  Chir.,  1907,  3  Suppl. 


30  DISEASES  OF  THE  BRONCHI 

complete.  In  1009  Eicken1  increased  the  number  to  303.  Brunings'2 
bronchoscope  is  the  instrument  most  commonly  used. 

Etiology. — Foreign  bodies  which  gain  entrance  to  the  air  passages 
are  of  endless  variety,  but  consist  for  the  most  part  of  small  articles 
commonly  placed  in  the  mouth. 

Aspiration  usually  takes  place  during  an  unexpected,  forced  inspira- 
tion, such  as  may  accompany  a  sudden  impulse  to  cough,  laugh,  or 
cry,  a  fright,  or  a  blow  on  the  back.  It  may  also  occur  while  the 
patient  is  asleep,  intoxicated,  partially  or  completely  unconscious 
from  narcosis  or  other  cause.  Bones,  beans,  needles,  and  hollow 
bodies  are  the  most  frequent  invaders,  and  more  than  half  the  cases 
occur  in  children  under  five. 

The  mechanism  of  ready  entrance  and  difficult  exit  of  foreign  bodies 
has  been  compared  to  that  of  a  penny  savings-box,  but  is  somewhat 
more  complicated.  Entrance  into  and  lodgement  in  the  air  passages 
are  facilitated  by  gravity  and  inspiratory  widening  of  the  glottis  and  the 
bronchial  tubes.  The  chances  of  spontaneous  expulsion  are  diminished 
by  expiratory  narrowing  of  the  passages  and  reflex  spasmodic  closure 
of  the  glottis,  so  that  expiratory  efforts  are  relatively  ineffectual,  and, 
even  if  successful,  exit  through  the  glottis  may  not  be  possible.  Par- 
tial absorption  of  air  below  an  occluding  body  and  an  increase  of  pres- 
sure above  it,  during  spasmodic  attacks  of  cough  with  the  glottis 
closed  at  the  beginning  of  expiration,  may  more  firmly  fix  it  in  position. 
If  released  and  unexpelled  there  is  danger  of  reimpaction,  which, 
owing  to  the  diminished  inspiratory  current  into  a  previously  in  vol  ved 
territory,  is  likely  to  take  place  into  another  bronchus,  with  the  danger 
of  immediate  suffocation. 

The  conditions  differ  according  to  the  character  of  the  foreign 
body.  Beans  capable  of  swelling  are  likely  to  completely  occlude  the 
bronchus,  and  are  difficult  to  extract,  hence  most  dangerous.  Hough 
bodies  of  an  irregular  shape,  such  as  pieces  of  bone,  are  likely  to  be 
held  in  place.  Hollow  bodies  may  permit  the  passage  of  air,  but  make 
expulsive  efforts  ineffectual.  Needles  become  quickly  fixed,  but  allow 
air  to  pass  readily  to  and  fro  and  cause  less  severe  initial  symptoms. 
The  larger  the  foreign  body  and  the  smaller  the  child  the  greater  the 
danger  of  suffocation. 

The  bronchi  leading  to  the  lower  lobes  are  usually  invaded,  and  the 
right  side  in  about  80  per  cent,  of  the  cases.  The  likelihood  of  right- 
sided  invasion  increases  with  the  youth  of  the  patient.  The  greater 
aspiratory  force  of  the  right  lung,  the  more  vertical  course  and  larger 
size  of  the  right  primary  bronchus  serve  to  explain  the  greater  frequency 
of  lodgement  on  the  right. 

Pathology. — Bacteria  invariably  accompany  aspirated  foreign  bodies, 
and  are  largely  responsible  for  the  pathologic  changes.    Much  depends 

1  Die  directe  Laryngo-Tracheo-Bronchoskopie,  Deut.  Klinik,  vol.  xii. 

2  Deut.  med.  Woeh.,  16  Mai,  1912. 


ASPIRATED  FOREIGN  BODIES  31 

on  the  interval  which  elapses  after  the  aspiration.  Within  the  first 
few  hours,  unless  death  occurs  from  suffocation,  the  local  changes  are 
limited  to  erosion  and  simple  inflammatory  swelling  of  the  mucous 
membrane.  Such  lesions  are  quickly  repaired  following  successful 
removal.  At  times,  however,  grave  inflammatory  processes  develop 
with  astonishing  rapidity,  and  in  rare  instances  pneumonia  may  follow 
within  twenty-four  hours.  If  the  foreign  body  remains  impacted, 
purulent  bronchitis,  ulceration  of  the  bronchial  wall,  extension  of 
inflammation  to  the  peribronchial  and  neighboring  pulmonary  tissue 
usually  occur.  Complete  bronchial  occlusion  is  followed  by  absorption 
of  air  and  atelectasis  in  the  involved  territory,  and,  whether  partial 
or  complete,  infection  soon  leads  to  multiple  or  confluent  areas  of 
bronchopneumonia  and  to  bronchiectasis.  Disintegration  of  tissue, 
weakening  or  ulceration  of  the  bronchial  wall,  and  the  accumulation 
of  purulent  secretion  below  the  obstruction  usually  reopen  the  occluded 
passage,  and  may  even  partially  dislodge  or  extrude  the  foreign  body. 
By  extension,  aspiration,  or  metastasis,  acute  or  subacute  broncho- 
pneumonia is  likely  to  arise  in  nearby  or  remote  parts  of  the  same  or 
the  other  lung.  Chronic  interstitial  pneumonia,  multiple  areas  of 
abscess,  gangrene  and  bronchiectasis  are  likely  to  follow.  In  rare 
instances,  tuberculosis  or  actinomycosis  develops.  The  foreign  body 
may  be  discharged  through  the  chest  wall.  Fibrinous,  serofibrinous, 
or  purulent  pleurisy  and  pneumothorax  are  occasionally  observed. 
These  chronic  and  permanently  damaging  processes  may  be  avoided 
by  immediate  removal  or  spontaneous  expulsion  of  the  foreign  body. 

Symptoms. — These  may  be  divided  into  primary  and  secondary 
manifestations,  between  which  a  period  of  comparative  latency  may 
intervene. 

Immediately  following  the  aspiration,  severe  symptoms  due  to 
irritation  and  suffocation  may  be  observed.  There  are  paroxysmal 
cough,  spasm  of  the  glottis,  inspiratory  and  expiratory  dyspnea,  a 
sense  of  suffocation  and  cyanosis.  The  severe  cough  and  dyspnea 
gradually  diminish  in  intensity  and  commonly  last  only  a  few  hours, 
but  may  unexpectedly  recur  at  intervals.  Persistence  of  dyspnea 
without  cough  usually  indicates  that  the  foreign  body  has  become 
fixed.  Hoarseness  may  be  present  if  the  vocal  cords  have  been  injured 
or  if  the  body  is  situated  in  their  neighborhood.  A  sense  of  irritation 
in  the  sternal  region  or  deep  in  the  chest  is  common,  but  actual  pain 
is  infrequent,  although  it  may  occasionally  be  observed  with  sharp 
or  pointed  bodies,  and  is  then  usually  thoracic,  in  rare  instances  it  is 
abdominal.  Sputum  is  absent  or  scanty  and  at  times  blood-tinged. 
If  the  body  is  large  or  movable,  paroxysms  of  cough  and  dyspnea  may 
be  of  extreme  severity,  with  suffocation,  strangling,  vomiting,  con- 
vulsions, attacks  of  unconsciousness,  or  death.  A  fatal  termination 
immediately  after  the  aspiration  is,  however,  fortunately  uncommon. 

After  the  subsidence  of  the  initial  symptoms,  if  the  foreign  body 
remains  impacted,  a  period  of  comparative  relief  usually  follows,  and 


32  DISEASES  OF  THE  BRONCHI 

the  patient  may  be  troubled  only  by  occasional  slight  cough  and 
dyspnea  on  exertion.  This  interval  of  partial  or  complete  relief  often 
leads  to  a  false  sense  of  security,  but  is  followed  usually  within  a  few 
days  by  secondary  manifestation  of  pulmonary  infection.  Cough,  more 
or  less  abundant,  purulent  and  foul-smelling  sputum,  fever,  and  such 
other  symptoms  as  are  common  with  bronchitis,  bronchial  and  pul- 
monary suppuration  ensue,  and  continue  for  an  indefinite  period. 
The  chronic  stage  may  last  weeks,  months,  or  years,  and  when  death 
occurs  it  is  usually  due  to  sepsis. 

In  Neumeyer's1  case  the  extraction  of  a  bone  twenty-four  hours 
after  aspiration  did  not  prevent  pneumonia,  which  proved  fatal  in 
the  next  twenty-four  hours.  In  one  of  Gottstein's2  cases  pneumonia 
developed  in  forty-eight  hours  after  aspiration  of  a  needle. 

The  initial  symptoms  may  be  insignificant,  overlooked,  misinter- 
preted or  forgotten,  and  the  foreign  body  remain  unrecognized  as  the 
cause  of  an  apparent  simple  bronchitis,  bronchopneumonia,  bronchiec- 
tasis, abscess,  gangrene,  or  empyema.  In  Carpenter's''  patient,  such 
insignificant  symptoms  followed  the  aspiration  of  four  artificial  teeth 
that  the  patient  thought  they  had  passed  in  the  stool,  but  they 
were  found  at  autopsy  thirteen  years  later  in  the  pus  of  an  empyema. 
Leyden4  reported  two  unsuspected  instances  in  physicians,  one  of 
whom  had  symptoms  suggestive  of  chronic  tuberculosis,  which  was 
found  at  autopsy  to  be  due  to  an  aspirated  bone.  The  other  was  an 
invalid  from  severe  cough  and  gangrenous,  putrid  sputum,  the  cause 
of  which  wTas  uncertain  until  in  a  severe  paroxysm  of  cough  a  shirt- 
button  was  expelled. 

In  rare  instances  a  body  too  large  for  impaction  in  the  bronchi  is 
aspirated  through  the  glottis,  and  may  then  remain  free  and  mobile 
in  the  air  passages,  or  it  may  happen  that  a  body  expelled  from  the 
bronchus  is  too  swollen  for  reimpaction  and  likewise  remains  free. 
Such  mobile  dancing  bodies  may  oscillate  back  and  forth  between  the 
glottis  and  the  bifurcation  of  the  trachea,  causing  paroxysms  of  cough 
of  extreme  severity  and  attacks  of  suffocation.  Lodgement  of  toy 
whistles  in  the  air  passages  may  result  in  squeaks  or  whistling  sounds 
with  inspiration  or  expiration.  In  Andrew's5  case  the  aspiration  of  a 
toy  squeaker  was  followed  by  a  short,  shrill  inspiratory  whistling  sound. 

Signs. — In  cases  in  which  the  lodgement  is  in  the  larynx  or  trachea, 
examination  of  the  lungs  is  usually  negative.  Invasion  of  the  principal 
bronchi  or  their  branches  commonly  gives  important  indications. 
Total  occlusion  of  a  principal  bronchus  causes  markedly  diminished 
respiratory  motion,  diminished  or  absent  diaphragm  shadow  (Litten's 
phenomenon),  breath  sounds,  voice,  whisper,  and  tactile  fremitus  on 
the  affected  side.  The  percussion  note  is  unchanged  or  at  times  tym- 
panitic in  quality.    Percussion  of  the  pulmonary  margin  during  forced 

1  Munch,  med.  Woch.,  1904,  38  and  39,  case  6. 

*  Loc.  cit.  3  Guy's  Hosp.  Rep.,  1842,  vii,  353. 

4  Deut.  med.  Woch.,  1903,  V.  B,  p.  34.  6  Lancet,  1903,  i,  1296. 


ASPIRATED  FOREIGN  BODIES 


33 


inspiration  and  expiration  shows  absence  of  mobility.  Fever  is  absent. 
Obstruction  of  a  branch  of  the  principal  bronchus  may  be  indicated 
by  similar  signs  limited  to  the  involved  territory.  If  the  occlusion  is 
partial  the  signs  are  correspondingly  less  marked,  and  if  the  object 
is  small  and  allows  free  passage  of  air  to  and  fro,  nothing  may  be  found 
except  perhaps  slight  limitation  of  motion  on  forced  breathing  from 
reflex  irritation  on  the  affected  side.  In  some  cases,  sibilant  or 
sonorous  sounds  may  be  heard,  of  maximum  intensity  over  the  site 
of  the  partial  obstruction. 

Fig.  2 


Stick  pin  in  bronchus.     (Gottstein.) 

X-ray  Examination. — This  is  an  important  method,  and  may  be  indis- 
pensable in  doubtful  or  difficult  cases.  It  is  specially  useful  in  deter- 
mining the  presence  and  position  of  metallic  bodies.  Of  156  cases 
collected  by  Eicken1  metallic  bodies  were  thus  demonstrated  in  all  but 


1  Zeit.  f.  Ohrenheilk.  u.  f.  d.  Krank.  d.  Luftwege,  Band  lxv,  Heft  2  u.  3,  p.  103. 
3 


34  DISEASES  OF  THE  BRONCHI 

five.  It  is  less  valuable  for  the  demonstration  of  bone  and  ivory 
substances,  a  positive  result  being  obtained  among  40  such  cases  in 
only  4,  in  all  of  which  the  body  was  of  considerable  size,  and  so  for- 
tunately placed  as  to  appear  as  a  shadow  in  an  intercostal  space. 
Even  when  the  foreign  body  itself  cannot  be  demonstrated,  evidence 
of  considerable  value  may  still  be  obtained.  A  shadow  from  changes 
in  the  pulmonary  tissue  about  the  body  may  be  noted.  The  intercostal 
space's  may  be  narrowed  and  the  diaphragm  elevated  on  the  affected 
side  in  consequence  of  pulmonary  retraction.  Dislocation  of  the  medi- 
astinum toward  the  involved  region  may  be  observed.  Radiographs 
should  be  taken  with  the  breath  held  in  full  inspiration.  Fluoroscopic 
examination  may  show  limited  respiratory  excursion  of  the  chest  wall 
and  the  diaphragm  and  with  a  hard  cough  expiratory  dislocation  of  the 
mediastinum  toward  the  involved  lung.  A  body  in  the  esophagus 
may  be  indicated  by  a  median  position  and  motion  on  swallowing, 
but  not  with  respiration.  Lateral  position  and  mobility  with  respira- 
tion suggest  lodgement  in  the  lung.  With  the  x-ray  plate  on  the  back 
the  size  of  the  projected  shadow  is  more  nearly  that  of  the  foreign 
body  if  it  lies  in  the  esophagus,  relatively  larger  if  more  anteriorly 
placed  in  a  bronchus.    Stereoscopic  plates  may  assist  in  the  localization. 

Diagnosis. — This  is  easily  made  if  there  is  a  definite  history  of 
aspiration,  the  immediate  occurrence  of  paroxysmal  cough  and  dysp- 
nea, and  signs  of  partial  or  complete  occlusion  of  a  bronchus.  It  is 
important  to  know  the  size,  shape,  and  kind  of  foreign  body,  and  it  is 
well,  if  possible,  to  obtain  another  article  of  the  same  sort.  In  children 
and  in  adults  when  the  aspiration  occurs  during  partial  or  complete 
unconsciousness  there  may  be  nothing  in  the  history  to  suggest  a 
foreign  body.  In  such  cases,  and  in  those  in  which  the  initial  symptoms 
are  slight,  atypical,  or  absent,  the  diagnosis  is  difficult.  Foreign 
bodies  should  be  suspected  in  all  cases  in  which  there  is  circumscribed 
bronchopneumonia,  bronchiectasis,  abscess  or  gangrene  of  uncertain 
origin,  and  especially  when  the  right  lower  lobe  is  involved. 

Not  infrequently  with  children,  and  at  times  with  adults,  the  patient 
is  said  to  have  "swallowed  something"  or  "choked."  If  the  body  is 
lodged  in  the  esophagus  there  is  likely  to  be  increase  of  saliva,  and 
difficulty  and  pain  on  swallowing  solid  food,  but  no  cough  or  dyspnea. 
Paroxysmal  cough  and  dyspnea,  absence  of  pain  and  ability  to  swallow, 
suggest  aspiration  into  the  air  passages.  Examination  with  the  .r-ray 
may  assist  in  the  differentiation.  In  rare  instances  an  attack  of  spas- 
modic laryngitis,  laryngeal  diphtheria,  whooping  cough,  or  asthma  may 
be  mistaken  for  aspiratiorr  of  a  foreign  body. 

A  foreign  body  lodged  in  the  esophagus  may  perforate  the  wall  and 
lead  to  pulmonary  symptoms.  It  may  then  be  difficult  to  determine 
whether  the  foreign  body  is  in  the  esophagus  or  the  air  passages.  A 
history  of  dysphagia  and  the  absence  of  initial  pulmonary  symptoms 
are  of  importance  in  the  differentiation.  In  the  case  of  A.  C.  (No.  192, 
934),  who  swallowed  a  chicken  bone,  there  was  constant  pain  on 


ASPIRATED  FOREIGN  BODIES  35 

swallowing.  He  began  to  cough  three  days  after  the  accident,  and  in 
the  following  six  weeks  had  fever  and  abundant,  foul-smelling,  purulent 
sputum  containing  elastic  tissue.  There  was  dulness  on  percussion 
and  a  shadow  by  x-ray  examination  (Chapter  XVI,  Fig.  44)  at  the 
root  of  the  right  lung.  The  bone  was  successfully  extracted  from  the 
esophagus.  The  patient  died  five  months  later  of  pulmonary  tuber- 
culosis. 

Spontaneous  expulsion  of  a  fragment  of  bone  is  not  an  assurance 
of  absence  of  other  fragments.  In  long-standing  cases  persistence  of 
paroxysmal  cough  and  signs  of  atelectasis  should  lead  to  the  suspicion 
that  a  foreign  body  may  still  be  present.  In  the  case  of  L.  K.,  aged 
sixty-six  years,  seen  with  Drs.  A.  Coolidge  and  H.  P.  Mosher,  May  1, 
1914,  there  was  a  history  of  aspiration  of  a  chicken  bone  nine  months 
before.  Severe  paroxysmal  cough  and  one  to  three  ounces  of  muco- 
purulent sputum  persisted  in  spite  of  the  expulsion  of  a  small  piece 
of  bone  thirteen  weeks  after  the  accident  Examination  showed  involve- 
ment of  the  root  of  the  right  lung  and  partial  atelectasis  of  the  right 
lower  lobe.  A  second  fragment  of  bone,  about  1  cm.  long  and  0.6 
cm.  in  greatest  diameter,  was  removed  by  bronchoscopy  from  one  of 
the  branches  of  the  right  primary  bronchus  on  May  16  by  Drs.  Coolidge 
and  Mosher.  The  patient  developed  a  left  hemiplegia  during  the  opera- 
tion. On  the  third  day  after  operation  he  coughed  up  a  third  fragment 
of  bone,  about  0.6  cm.  long,  sharp  and  pointed  at  one  extremity  and 
irregularly  club-shaped  at  the  other,  the  greatest  diameter  reaching 
0.2  cm.  Cough  and  expectoration  rapidly  subsided.  On  June  4  the 
expectoration  amounted  to  only  three  or  four  small  masses  of  mucopus 
a  day.    The  hemiplegia  persisted. 

Of  great  importance  in  diagnosis  is  the  use  of  the  bronchoscope. 
Among  137  cases  collected  to  April  1,  1906,  by  Gottstein1  a  diagnosis 
was  successfully  made  by  this  means  in  121  (88.3  per  cent.).  The 
failure  to  establish  the  diagnosis  in  16  (11.6  per  cent.)  cases  may  be 
largely  ascribed  to  faulty  technique  early  in  the  use  of  this  method. 

Prognosis. — Recovery  seldom  occurs  unless  the  foreign  body  is 
spontaneously  expelled  or  extracted.  Encapsulation  and  freedom 
from  symptoms  with  the  body  remaining  only  rarely  occurs. 

Spontaneous  expulsion  occurs  in  a  not  inconsiderable  number  of 
cases,  but  the  expectation  of  relief  by  this  means  cannot  be  estimated 
with  sufficient  accuracy  in  individual  cases  to  justify  delay  in  treatment. 
Large,  soft  bodies  of  organic  material,  such  as  meat  or  fruit,  cause 
death  unless  immediately  expelled  or  extracted.  Smaller  particles 
may  quickly  undergo  disintegration,  and  may  be  successfully  expec- 
torated. Of  other  substances,  according  to  Gottstein,2  rough,  jagged 
bodies,  such  as  bone,  and  smooth,  flat,  or  smooth,  round  and  even 
pointed  bodies,  are  expelled  in  about  one-third  of  the  cases,  while 
those  which  swell  by  imbibition,  such  as  beans,  and  also  hollow  bodies 

1  Loc.  cit.  2  Loc.  cit. 


36  DISEASES  OF  THE  BRONCHI 

in  only  about  11  to  12  per  cent.  Much  depends  on  the  interval  which 
elapses  between  aspiration  and  removal.  Although  expulsion  not  infre- 
quently follows  in  the  course  of  secondary  pulmonary  suppuration,  it 
usually  fails  to  relieve  the  chronic  inflammatory  changes  which  slowly 
progress  and  commonly  lead  to  a  fatal  termination.  In  most  cases 
in  which  complete  relief  follows  the  expulsion  the  foreign  body  has 
been  fixed  in  the  upper  part  of  the  air  passage  and  not  in  the  bronchi. 

Progress  in  the  development  and  use  of  the  bronchoscope  has 
greatly  increased  the  prospect  of  successful  removal  and  avoidance 
of  dangerous  secondary  infection. 

Of  114  cases  collected  by  Gottstein,1  in  which  the  diagnosis  of  the 
presence  of  a  foreign  body  was  established  by  the  bronchoscope, 
bronchoscopic  extraction  was  completely  successful  in  96  (84  per  cent.). 
Of  113  cases  in  which  the  outcome  was  known,  97  (86  per  cent.)  were 
"cured/'  9  died  in  spite  of  the  removal,  and  7  died  without  the  foreign 
body  having  been  removed. 

Of  231  cases2  collected  by  Eicken,3  177  were  completely  and  29 
partially  relieved,  while  the  attempt  was  unsuccessful  in  25  cases. 

Treatment. — In  acute  cases  the  chances  of  spontaneous  expulsion 
do  not  justify  delay.  Postponement  may  be  followed  by  sudden  death 
in  the  interval,  as  in  Schlender's4  patient,  a  boy,  aged  three  years, 
who  had  aspirated  a  cartridge  case,  showed  no  alarming  symptoms, 
and  was  to  be  operated  the  next  day,  but  died  in  the  night  in  an  attack 
of  suffocation.  No  time  should  be  lost.  Cough  should  not  be  excited, 
and  such  customary  procedures  as  a  blow  on  the  back,  shaking  the 
patient  and  the  use  of  emetics  should  be  avoided  lest  the  body  become 
more  firmly  impacted  or  expelled  from  its  original  position  and  reaspi- 
rated  into  another  bronchus.  The  effect  of  posture  may  be  tried  while 
making  ready  for  the  extraction,  the  patient  lying  with  his  face  toward 
the  floor  and  the  body  so  inclined  that  the  bronchi  slope  downward 
in  the  hope  that  gravity  may  assist  in  the  expulsion.  Examination 
for  a  foreign  body  in  the  pharynx  and  larynx  should  first  be  made  and 
the  body  extracted  with  the  finger  or  forceps,  assisted,  if  necessary,  by 
inspection  with  the  laryngeal  mirror. 

In  chronic  cases  an  attempt  should  be  made  even  though  a  long 
interval  has  elapsed  since  the  aspiration  of  the  foreign  body.  In  one 
of  Jackson's5  two  remarkable  cases  the  removal  by  bronchoscopy, 
of  a  collar-button,  lodged  for  ten  years  in  the  right  bronchus  was 
followed  by  complete  recovery  and  freedom  from  any  pulmonary 
symptoms  whatever.  In  his  second  case  the  removal  from  the  right 
bronchus  of  a  price-tag  fastener,  aspirated  seven  years  previously, 
was  likewise  followed  by  complete  relief. 

1  Loc.  cit. 

2  Bronchial  cases  have  been  abstracted  from  his  table. 

*  Deut.  Klinik,  Band  xii  and  Int.  Zentbl.  f.  Laryngol.,  1909,  Jahrg.,  xxv,  p.  554. 

4  Deut.  Zeit.  f.  Chir.,  Band  lxiv,  p.  411. 

5  Jour.  Amer.  Med.  Assoc,  September  21,  1912. 


ASPIRATED  FOREIGN  BODIES 


37 


Bronchoscopy.1 — Although  Voltolini,2  Pieniazek,14  and  others  used 
this  method,  to  Killian4  belongs  the  credit  of  developing  and  making 
it  practical.  Coolidge5  was  the  first  to  report  the  use  of  the  broncho- 
scope in  America.  Gottstein6  and  Eicken7  have  recently  reviewed  the 
literature. 

Fig.  3 


Bronchoscopy.      (Briinings.) 

The  bronchoscope8  consists  of  a  long,  stiff,  metal  tube  mounted  on 
a  handle,  an  illumination  apparatus,  and  extracting  forceps  of  various 
types.  The  instrument  is  introduced  through  the  mouth  and  larynx 
(upper  tracheobronchoscopy)  or  through  a  tracheotomy  wound  (lower 
tracheobronchoscopy).  The  former  method  presents  many  technical 
difficulties  and  requires  skill  and  practice.  General  or  local  anesthesia 
is  used.  Tracheotomy  is  recommended  when  there  is  severe  dyspnea 
or  with  a  body  so  large  as  to  be  extracted  through  the  glottis  only 
with  difficulty.  The  upper  route  (upper  tracheotomy)  is  to  be  pre- 
ferred over  the  lower.  Aortic  aneurysm  and  severe  cardiac  decom- 
pensation are  contra-indications.  Slight  bleeding,  edema  of  the 
larynx,  and  aphonia  may  follow  upper  tracheobronchoscopy.  Emphy- 
sema may  develop  after  lower  tracheobronchoscopy. 


1  For  technical  details,  special  works  must  be  consulted. 

2  Berl.  klin.  Woch.,  1875,  p.  71. 

3  Arch.  f.  Laryngol.,  1896,  Band  v,  p.  210. 

4Kallofrath,   Munch,  med.  Woch.,    1897,   p.    1038;    Killian,   Munch,  med.  Woch., 
1899;   Deut.  med.  Woch.,  August  31,  1911. 
6  New  York  Med.  Jour.,  September  30,  1899. 

6  Mitt.  a.  d.  Grenzg.  d.  Med.  u.  Chir.,  1907,  3  Suppl. 

7  Deut.  Klinik,  xii,  and  Int.  Zentbl.  f.  Laryngol.,  1909,  xxv,  554. 

8  See  Gottstein,  loc.  cit. ,    Jackson,  Laryngoscope,  St.  Louis,   1908,  xviii,  214;  and 
Brunings,  Deut.  med.  Woch.,  16  Mai,  1912. 


38 


DISEASES  OF   THE  BRONCHI 


Other  Methods. — In  case  bronchoscopy  fails,  such  other  procedures 
as  intrathoracic  Cracheotomy,  bronchotomy  by  way  of  the  posterior 


Fig.  4 


Fig. 


Bronchoscopy.     (Briinings.) 


Universal   electroscope   for 
lower    tracheobronchoscopy. 

(Briinings.) 


Fig.  6 


Extracting  f orceps."_  (Briinings.) 


FOREIGN  BODIES  ARISING  FROM  WITHIN  39 

mediastinum,  or  pneumobronchotomy,  under  positive  (Brauer's 
method1)  or  negative  pressure  (Sauerbruch's  method2)  may  be  con- 
sidered, but  as  yet  have  only  rarely  proved  successful . 


6.  FOREIGN   BODIES   ARISING   FROM   WITHIN. 

Under  this  heading  may  be  described  foreign  bodies  in  the  air  pas- 
sages and  the  lung,  for  the  most  part  the  result  of  pathologic  changes 
and  capable,  when  dislodged  from  their  site  of  formation,  of  giving 
rise  to  such  manifestations  as  have  been  considered  in  the  preceding 
section.     Poulalion3  collected  and  reviewed  the  literature  at  length. 

Etiology  and  Pathology. — In  a  large  proportion  of  the  cases  these 
bodies  consist  of  caseous  or  calcified  masses,  developing  in  the  course  of 
chronic  tuberculosis  of  the  lung  or  bronchial  lymph  glands,  and  gaining 
entrance  to  the  air  passages  by  inflammatory  softening  and  ulceration 
of  the  surrounding  and  supporting  tissue.  The  inspissated  contents 
of  pulmonary  cavities  or  bronchiectases,  the  pus  of  an  old  empyema, 
retained  blood-clot,  fragments  of  bronchial,  pulmonary  or  pleural 
tissue,  bits  of  tumor  or  hydatids  may  also  become  infiltrated  with 
lime  salts  and  expelled  into  the  bronchi.  In  rare  instances  an  aspirated 
foreign  body  is  incrusted  with  lime  salts  and  extruded. 

In  some  instances  the  deposition  of  lime  salts  takes  place  over  a 
wider  extent  of  tissue  and  in  connection  with  less  obvious  inflammatory 
changes.  In  old  persons  petrifaction  of  the  bronchi  with  the  formation 
of  coral-like  and  branching  structures  occurs  as  in  the  case  described 
by  Andral.4  A  diffuse  incrustation  of  the  pulmonary  tissue  may  also 
be  observed.  Local  circulatory  disturbances  and  diminished  vitality 
of  the  tissue  in  consequence  of  venous  stasis  from  cardiac  failure, 
embolism,  or  thrombosis,  as  suggested  by  Kockel,5  may  be  responsible 
for  the  deposition  in  the  affected  region.  A  constitutional  anomaly 
has  also  been  assumed,  but  seems  a  less  likely  explanation. 

The  cartilages  of  the  trachea  or  bronchi  or  small  masses  of  bone 
arising  by  metaplasia  of  cartilage  or  connective  tissue  in  any  part  of 
the  respiratory  tract6  may  be  freed  by  ulceration  and  expelled.  In 
the  course  of  destructive  pulmonary  processes,  such  as  ulcerative 
tuberculosis,  abscess  or  gangrene,  fragments  of  lung  tissue,  and  in 
pneumonoconiosis  fragments  of  lung  impregnated  with  inhaled  dust 
may  be  expectorated. 

Adhesion  of  caseous,  calcified  or  anthracotic  bronchial  glands  to  the 

1  Mitt.  a.  d.  Grenzg.  d.  Med.  u.  Chir.,  1904,  Band  xiii,  p.  482. 

2  Ibid.,  p.  399. 

3  Les  pierres  du  poumon,  de  la  plevre  et  des  bronches  et  la  pseudophthisie  pulmonaire 
d'origine  calculeuse,  These  de  Paris,  1891. 

4  Clin,  med.,  1837,  T.  ii,  p.  109. 

5  Deut.  Arch.  f.  klin.  Msd.,  Band  Ixiv,  p.  332. 

6  See  Pollak,  Virchow's  Arch.,  Band  clxv,  p.  168;  Sippel,  TJeber  Knoehenbildung  in 
Bronchiektasen,  Frankfurter  Zeit.  f.  Path.,  1910-11,  6. 


40  DISEASES  OF  THE  BRONCHI 

bronchi  may  be  followed  by  ulceration  and  perforation  of  the  inter- 
vening wall.  Among  6132  autopsies,  Sternberg1  noted  the  perforation 
of  softened  bronchial  glands  in  19  cases  into  the  bronchus  (14  into  the 
right  and  5  into  the  left  bronchus)  and  esophagus,  in  1  into  the  left 
bronchus  and  the  aorta,  in  3  into  the  bronchi  (in  one  with  coincident 
perforation  of  a  second  gland  into  the  esophagus),  in  1  into  the  trachea 
and  esophagus,  and  in  3  into  the  trachea  alone. 

In  1902  Schaldemose2  collected  19  cases  and  added  1  of  his  own  in 
which  caseous  glands  had  perforated  into  the  air  passages.  A  number 
of  cases  have  since  been  reported.  Children  are  principally  concerned. 
Various  consequences  may  follow.  The  gland  may  be  spontaneously 
expelled,  with  complete  recovery,  as  in  Jundell's3  unusual  case,  par- 
tially extruded  with  incomplete  or  total  occlusion  of  the  bronchus  or 
impacted  in  the  trachea  or  glottis,  causing  sudden  death  by  suffoca- 
tion. The  inhalation  of  infected  material  may  lead  to  local  or  wide- 
spread pulmonary  tuberculosis  or  putrid  bronchitis,  bronchopneumonia, 
and  pulmonary  gangrene. 

Expectorated  calcareous  masses  are  more  common  in  adults  than 
in  children,  and  may  vary  from  a  single  one  to  several  hundred. 
Boerhaave4  states  that  Sebastianus  Vaillantius,  a  famous  botanist, 
expectorated  400  stones  before  his  death.  In  Stern's5  case  twenty  were 
expectorated  at  one  time.  They  vary  in  size  usually  from  that  of  a 
pin's  head  to  a  pea,  are  grayish  or  yellowish  white  in  color,  soft  and 
friable  or  of  stony  hardness,  and  of  an  irregular  shape,  with  a  rough, 
uneven,  or  coral-like  surface.  At  times  they  are  of  very  foul  odor. 
On  section  they  present  a  lamellated  or  homogeneous  structure. 
After  decalcification  in  nitric  acid,  hardening  in  alcohol,  and  imbedding 
in  paraffin,  stained  sections  usually  show  only  a  structureless,  homo- 
geneous mass  of  detritus.  In  cases  reported  by  Stern6  and  Biirgi,7 
tubercle  bacilli  were  demonstrated  in  the  masses.  Chemical  analysis 
usually  shows  calcium  phosphate  and  carbonate  as  principal  con- 
stituents, with  also  at  times  traces  of  magnesia.  In  Gerhartz  and 
Strigel's8  case  the  composition  was  calculated  to  be  61.29  per  cent. 
Ca(P04)2,  23.42  per  cent.  CaC03,  and  5.96  per  cent.  MgC03,  with 
9.33  per  cent,  nitrogen  containing  organic  substance. 

Symptoms  and  Signs. — The  symptoms  are  usually  those  of  chronic 
pulmonary  tuberculosis  or  suppuration,  in  the  course  of  which  a  small 
caseous  or  calcified  mass  or  a  fragment  of  pulmonary  tissue  is  expelled 
without  significant  manifestations,  and  first  discovered  by  chance 

1  Ueber  die  Erwiechung  bronchialer  Lymphdriisen  und  ihre  Folgen.,  Verhandl.  d. 
deutschen  path.  Gesellsch.,  1904-05,  7-9. 

2  Hospitalstidende,  4  Riikke,  Band  x,  p.  562. 

3  Spontane  Perforation  einer  tuberkiilosen  Bronchialdriise  in  die  Luftwege,  spontane 
Expektoration  derselben,  Genesung,  Jahrbuch  f.  Kinderheilk.,  1904,  lx,  76. 

4  Praelectiones  Academicse,  Editit  A.  Haller,  T.  vi,  Gottingre,  mdccxliv,  p.  121. 

5  Deut.  med.  Woch..  1904,  No.  39,  p.  1414. 

6  Loc.  cit.,  6rst  case.  7  Ibid.,  1906,  i,  32,  second  case. 
8  Beitrage  z.  Klinik  d.  Tub.,  1908,  10. 


FOREIGN  BODIES  ARISING  PROM  WITH  IN 


41 


during  an  examination  of  the  sputum.     Larger  masses  may  be  felt 
to  pass  through  the  glottis.      In  rare  instances  the  presence  in  or 


Fig.  7 


Specimens  of  calcareous  concretions  expectorated  by  Poulalion's  patient  No.  32.      X  4. 

passage  through  the  air  passages  of  a  calcified  mass  causes  striking 
and  characteristic  symptoms,  to  which  the  term  "bronchial  colic" 
or  "stone  asthma"  has  been  applied. 


42  DISEASES  OF  THE  BRONCHI 

During  the  attack  the  patient  may  complain  of  a  feeling  of  weight, 
pressure,  burning  or  cutting  pain  referred  to  the  lower  sternal  region 
or  other  part  of  the  chest,  with  spasmodic  and  severe  cough  and 
dyspnea.  Fever  may  accompany  and  follow  the  attack.  One  or 
more  stones  may  be  expelled  during  the  paroxysm,  which  may  last  for 
a  variable  period,  in  one  of  Poulalion's1  cases  for  nearly  forty-eight 
hours.  Small  amounts  of  blood  may  appear  in  the  sputum,  and  the 
stone  when  expectorated  may  be  blood-stained.  In  Cazeau's2  case  an 
accompanying  hemoptysis  was  fatal.  Ordinarily  the  expectoration 
of  the  stone  exerts  no  important  influence  on  the  course  of  the  under- 
lying disease.  At  times,  however,  more  abundant  sputum  may  follow, 
or  attacks  of  cough  and  expectoration  cease,  the  patient  remaining 
thereafter  well,  or  an  interval  of  comparative  health  is  followed  by 
recurrence  of  symptoms  and  more  stones. 

The  perforation  of  bronchial  glands  into  the  bronchi  is  accompanied 
by  paroxysmal  cough,  dyspnea,  sense  of  suffocation,  and  cyanosis 
and  such  other  symptoms  as  occur  with  aspirated  foreign  bodies. 
x\ctual  pain  is  infrequent.  Impaction  in  the  glottis  or  trachea  is  fol- 
lowed by  death  from  suffocation,  as  in  the  cases  described  by  Lohler,3 
who  found  twenty  similar  instances  in  the  literature. 

The  physical  signs  are  those  of  the  underlying  condition,  to  which, 
if  a  bronchus  is  partially  or  completely  occluded,  such  features  as  have 
been  described  for  aspirated  foreign  bodies  may  be  added. 

Diagnosis. — The  clinical  features  may  be  sufficient  to  determine 
the  presence  of  a  foreign  body  in  the  air  passages,  but  it  is  seldom 
possible  to  establish  its  nature  and  origin  unless  there  is  a  history  of 
previous  and  similar  disturbance.  Calcified  lung  and  bronchial  stones 
may  appear  as  shadows  on  the  .r-ray  plate,  but  it  is  difficult  to  identify 
them  by  this  means  as  a  cause  of  existing  symptoms.  The  expectora- 
tion of  calcareous  masses  from  in  or  about  the  teeth,  the  crypts  of  the 
tonsil,  the  ventricles  of  the  larynx  or  the  nose  must  be  excluded.  A 
bronchial  gland  may  be  suspected  in  children  if  an  aspirated  foreign 
body  can  be  ruled  out.  The  diagnosis  of  a  bronchial  gland  as  the  cause 
of  the  symptoms  has  usually  been  first  made  at  autopsy,  but  in  the 
cases  described  by  Peterson,4  Fronz,5  Nachod6  and  Schaldemose7  it 
was  established  during  life  by  removal  of  portions  of  the  gland  by 
tracheotomy,  and  in  Jundell's8  case  by  spontaneous  expulsion  of  the 
mass.  A  sudden  suffocative  attack  from  partial  occlusion  of  the 
trachea  by  a  gland  is  not  unlike  an  attack  of  thymic  asthma,  and  the 
mode  of  death  from  this  cause  may  resemble  thymus  death. 

1  Loc.  cit.,  p.  185. 

2  Hemoptysie  foudroyante  d'origine  calculeuse,  Bull,  de  la  Soc.  anat.  de  Paris,  1837, 
T.  ix,  p.  100. 

3  Munch,  med.  Woch.,  1904,  li,  1205. 

4  Deut.  med.  Woch.,  1885,  p.  145. 

6  Two  cases,  Jahrb.  f.  Kinderh.,  1897,  N.  F.,  Bd.  xliv,  p.  1. 

6  Prag.  med.  Woch.,  1897,  p.  393. 

7  Hospitalstidende,  4  Riikke,  Band  x,  p.  562.  s  Loc.  cit. 


FOREIGN  BODIES  ARISING  FROM  WITIIfN  43 

Prognosis. — For  lung  and  bronchial  stones  which  are  expelled  the 
prognosis  is  that  of  the  underlying  disease,  which  is  tuberculous  in 
a  majority  of  the  cases,  and  of  which  the  foreign  body  may  be  regarded 
as  a  symptom.  Inasmuch  as  disintegration  of  tissue  is  ordinarily 
a  necessary  forerunner  of  dislodgement  of  the  stone,  its  appearance 
in  the  air  passages  may  be  regarded  as  an  indication  of  an  active 
disease.  Traumatic  and  inflammatory  lesions  may  follow  the  expul- 
sion, thus  adding  to  the  unfavorable  aspect  of  the  situation.  In  some 
cases,  however,  all  symptoms  subside  after  expectoration  of  a  stone 
The  outlook  is  not  favorable  with  perforation  of  bronchial  glands  into 
the  air  passages.  Much  depends  on  successful  treatment.  Fronz's 
2  cases  died  in  spite  of  tracheotomy,  but  successful  removal  by  this 
means  in  Peterson's,  Nachod's,  and  Schaldemose's  cases  and  spon- 
taneous expulsion  in  Jundell's  were  followed  by  recovery  in  spite  of 
the  presence  of  tubercle  bacilli  in  the  masses  in  two  of  the  four. 

Treatment. — In  most  cases  this  must  be  limited  to  measures  against 
the  underlying  disease.  The  encapsulation  of  and  deposition  of  lime 
salts  in  tuberculous  tissue  is  favorable  in  so  far  as  it  makes  the  local 
infection  obsolete  and  innocuous.  In  many  cases  mild  tuberculous 
invasion  is  cured  in  this  way,  and  it  has  even  been  suggested  that  an 
attempt  should  be  made  to  hasten  the  calcification  by  the  administra- 
tion of  calcium  salts.  The  dislodgement  and  expulsion  of  calcified 
areas  are  so  infrequent  as  to  make  the  dangers  incident  thereto  a 
minor  consideration  against  such  a  course  if  it  could  be  successfully 
carried  out.  Thus  far  greater  reliance  seems  justly  placed  on  hygienic- 
dietetic  measures.  Active  treatment  against  foreign  bodies  arising 
from  within  the  individual  is  required  only  in  cases  in  which  they 
give  rise  to  troublesome  symptoms,  and  is  most  urgent  when  the  air 
passages  are  obstructed.  Under  these  circumstances,  bronchoscopy 
with  or  without  tracheotomy  is  most  likely  to  prove  successful,  follow- 
ing the  indications  already  mentioned  in  the  preceding  section. 


CHAPTER   IT. 
BRONCHIAL  ASTHMA. 

Among  the  older  writers,  many  affections  with  paroxysmal  dyspnea 
were  classed  as  asthma.  The  existence  of  asthma  as  an  independent 
disease  was  denied  by  some  and  upheld  by  others.  Thus  Rostan, 
Beau,  Louis,  and  others  looked  upon  asthma  as  dependent  on  bronchial 
catarrh  or  emphysema.  Willis  suggested  a  connection  with  spasmodic 
constriction  of  the  bronchi,  but  did  not  differentiate  bronchial  and  car- 
diac asthma.  Laennec  connected  asthma  with  "catarrhe  sec"  and  other 
forms  of  bronchitis.  He  acknowledged  the  possibility  of  a  tonic  spasm 
of  the  bronchial  muscles,  and  believed  that  the  majority  of  asthmatic 
attacks  were  principally  due  to  an  alteration  of  nervous  influence. 
His  belief  would  thus  accord  well  with  the  present  view  of  asthma. 
Romberg  and  Bergson  especially  emphasized  the  idiopathic  nature  of 
the  disease.  The  existence  of  an  independent  affection,  unconnected 
with  obvious  disease  of  the  heart,  the  lungs,  or  other  organs  is  now 
generally  accepted,  and  principal  interest  centres  in  the  explanation 
of  the  paroxysms. 

The  disease  is  characterized  clinically  by  paroxysmal  attacks  of 
dyspnea  affecting  both  phases  of  respiration,  but  especially  expiration. 
The  attack  is  followed  by  cough  and  the  expulsion  of  a  tenacious, 
viscid  sputum.  During  the  attack  the  lungs  are  distended  and  the 
diaphragm  is  low.  Repeated  attacks  are  likely  to  lead  to  chronic- 
bronchitis  and  emphysema. 

Theories  of  Asthma. — As  yet  the  cause  of  the  disease  is  unknown. 
The  various  theories  may  be  grouped  under  (1)  spasm  of  the  bronchial 
muscles,  (2)  swelling  of  the  bronchial  mucous  membrane,  (3)  spasm 
of  the  diaphragm,  (4)  the  nervous  system  as  a  factor,  and  (5)  bronchial 
asthma  as  a  phenomenon  of  anaphylaxis. 

1.  Spasm  of  the  Bronchial  Muscles. — The  character  of  asthmatic 
dyspnea  suggests  an  obstruction  to  respiration.  The  apparent  freedom 
of  the  upper  respiratory  tract  and  the  lungs,  the  character  of  the  rales, 
and  the  caliber  of  the  Curschmann  spirals  suggest  that  this  obstruc- 
tion is  in  the  finer  divisions  of  the  bronchi.1  The  general  distribution 
of  the  rales  throughout  the  lungs  indicates  a  general  rather  than  a 
local  bronchial  involvement.  The  suddenness  of  onset  and  cessation 
of  asthmatic  paroxysms  may  be  regarded  as  an  argument  in  favor  of  a 

1  Riehl's  (Munch,  med.  Woch.,  1906,  p.  2240,  Nos.  46  and  47,  p.  2302)  cases  are 
exceptions.  Tn  the  sputum  of  each  of  four  patients  were  "giant"  spirals  from  6  to  24 
cm.  long  and  3  to  3.5  cm.  wide. 


BRONCHIAL  ASTHMA  45 

spasm  of  the  bronchial  muscles,  which,  on  theoretical  grounds,  would 
explain  the  paroxysms. 

This  theory  has  been  supported,  among  others,  by  Trousseau,1 
Romberg,2  Bergson,3  Salter,4  and  especially  by  Biermer,5  who  argued 
strongly  in  its  favor  and  showed  that  it  would  account  for  the  symp- 
toms of  the  disease. 

A  spasm  of  the  bronchial  muscles  would  obstruct  both  inspiration 
and  expiration.  It  would  account  for  the  greater  hindrance  to  expira- 
tion and  the  overdistention  of  the  lungs.  Owing  to  the  greater  force 
of  the  inspiratory  muscles,  the  resistance  to  inflation  is  more  readily 
overcome  than  that  offered  to  deflation.  Expiration,  moreover,  is 
accomplished  at  a  greater  mechanical  disadvantage,  for  in  consequence 
of  insufficient  deflation  the  alveoli  become  overdistended  and  the 
already  constricted  bronchioles  are  still  further  compressed  by  an 
increased  intrathoracic  pressure.  The  sibilant  and  sonorous  rales 
are  then  due  to  the  obstruction  offered  to  the  entrance  and  exit  of  air. 

The  structure  of  the  bronchial  muscles  is  not  at  variance  with  such 
an  hypothesis.  Aufrecht6  found  that  the  unstriped  musculature  of  the 
finer  bronchi  of  man  contains  a  thick,  strong  layer  of  circular  muscle 
fibers  and  a  much  weaker  layer  of  longitudinal  muscle  fibers.  Both 
are  intimately  interwoven.  The  normal  function  of  these  muscles  is 
unknown,  but  it  was  suggested  by  Biermer  that  they  are  antagonists 
of  the  inspiratory  muscles.  They  may  perform  a  protective  function, 
preventing  too  forcible  inspiratory  inflation  and  the  entrance  of  foreign 
bodies  or  irritating  substances  into  the  lungs.  It  is  also  possible  that 
they  play  a  part  in  forced  expiration  and  expectoration. 

Some  confirmation  of  the  bronchial  spasm  theory  of  asthma  is  found 
in  the  results  of  experimental  work.  Williams7  first  showed  that  the 
lungs  could  be  made  to  contract  by  passing  a  current  of  electricity 
through  them.  Of  the  various  experiments  since  performed  to  deter- 
mine the  innervation  of  the  bronchial  muscles,  those  of  Einthovens 
and  Beer9  are  noteworthy.  The  researches  of  Dixon  and  Brodie10 
are  of  special  interest.  From  their  experiments  it  is  shown  that  the 
bronchial  muscles  are  innervated  by  the  vagus  nerve,  which  contains 
both  bronchoconstrictor  and  bronchodilator  fibers.  The  sympathetic 
nerve  has  no  demonstrable  effect  on  the  bronchial  muscles.  By 
electrical  stimulation  of  the  vagus  they  were  able  to  demonstrate  a 
diminution  in  the  amount  of  air  entering  and  leaving  a  lobe  of  the  lung. 

The  clinical  observation  of  a  relation  between  affections  of  the  nose 
and  bronchial  asthma  received  support  by  their  experiments,  since 

1  Cliuique  medicale,  2  ed.,  ii,  p.  460. 

2  Lehrb.  d.  Nervenkrankh.,  Berlin,  1855,  3  Aufl. 

3  Das  krampfhafte  Asthma  der  Erwachsenen,  Nordhausen,  1850. 

4  On  Asthma,  London,  1850. 

5  Volkmann's  Samml.  klin.  Vortrage,  1870.  No.  3. 

6  Deut.  Arch.  f.  klin.  Med.,  1900,  Ixvii,  586. 

7  British  Assoc.  Reports,  1840.  p.  411.  8  Pfliiger's  Archiv,  1892,  li,  367. 

9  Arch.  f.  Anat.  u.  Physiologie,  1892,  Suppl.,  p.  101. 

10  Trans.  Path.  Soc,  London,  1903,  vol.  liv. 


■AG  DISEASES  OF   THE  BRONCHI 

electrical,  mechanical,  or  chemical  stimulation  of  the  nasal  mucous 
membrane  also  diminished  the  amount  of  air  entering  the  lung.  Stim- 
ulation of  the  upper  and  posterior  part  of  the  nasal  septum  was  most 
effective.  Section  of  the  vagus  entirely  abolished  the  result,  and  Mas 
followed  by  relaxation  of  the  reflex  constriction. 

It  cannot  be  said  that  the  experimental  data  substantiate  the  muscle 
spasm  theory  of  asthma.  It  does  show,  however,  that  spasm  of  the 
bronchial  muscles,  caused  either  by  direct  stimulation  of  the  vagus  or 
reflexly  through  the  nasal  mucous  membrane,  is  capable  of  causing 
an  obstruction  to  the  inflation  and  deflation  of  the  lung.  If,  as 
Striimpell1  suggests,  hypertrophy  of  these  muscles  could  be  shown  at 
autopsy  in  cases  with  asthma,  it  would  lend  support  to  the  view  of 
their  implication  as  a  cause  of  the  paroxysms.  Thus  far  this  has  not 
been  demonstrated. 

Certain  drugs  influence  the  bronchial  muscles.  The  bearing  of 
such  data  on  the  muscle-spasm  theory  is  not  easy  to  interpret.  Thus 
"muscarin,  pilocarpin,  physostigmin,  and  digitalin  produce  marked 
constriction  by  peripheral  stimulation  of  the  vagal  endings.  Gold 
salts,  barium  salts,  and  veratrin  produce  constriction  by  a  direct 
action  on  the  muscle  fibers.  Atropin,  hyoscyamin,  and  hyoscin 
paralyze  the  vagal  endings  and  thus  lead  to  dilatation  if  constriction 
is  present."  A  perfectly  typical  attack  of  asthma  can  be  produced 
in  an  animal  by  giving  it  a  small  dose  of  muscarin.  There  is  dyspnea, 
distention  of  the  lungs,  and  with  only  small  doses  no  excessive  secre- 
tion in  the  bronchi  and  bronchioles.  The  attack  thus  produced  can 
be  instantly  cut  short  by  an  injection  of  atropin.  Lobelia  produces 
a  transitory  relaxation  in  an  animal  in  which  bronchial  constriction 
has  been  produced  by  pilocarpin.  Morphin  also  tends  to  produce 
relaxation.  Chloroform  and  ether  paralyze  the  nerve  endings  and 
produce  relaxation.  (Brodie  and  Dixon.)  Januschke  and  Pollak2 
observed  a  widening  of  the  bronchial  lumen  under  the  influence  of 
adrenalin.  The  favorable  effects  of  atropin,  adrenalin,  lobelia,  mor- 
phin, chloroform,  and  ether  in  releasing  an  artificially  produced  bron- 
chial constriction  and  their  favorable  effect  in  asthma  in  man  suggest 
a  similarity  between  the  two  conditions. 

While  spasm  of  the  bronchial  muscles  as  a  cause  of  asthma  has 
much  in  its  support,  it  does  not  alone  satisfactorily  explain  the  prac- 
tically constant  presence  of  bronchial  secretion  unless  it  be  assumed 
that  this  also  is  due  to  the  bronchial  spasm.  It  is  difficult  to  under- 
stand how  this  can  be  the  case. 

2.  Swelling  of  the  Bronchial  Mucous  Membrane. — The  assumption 
that  the  bronchial  obstruction  is  due  to  swelling  of  the  mucous 
membrane  rather  than  to  spasm  of  the  bronchial  muscles  would  as 
satisfactorily  account  for  the  symptoms  of  asthma.  It  would  cause 
dyspnea  and,  for  reasons  similar  to  those  mentioned  under  Bronchial 

1  Med.  Klinik,  Berlin,  1908,  iv,  6-10. 

2  Arch.  f.  exp.  Path.  u.  Pharmakol.,  Band  lxvi. 


BRONCHIAL  ASTHMA  47 

Spasm,  would  lead  to  distention  of  the  lungs  and  low  position  of  the 
diaphragm.  An  obstruction  alone  would  account  for  the  rales,  but  an 
affection  of  the  mucous  membrane  more  satisfactorily  explains  the 
presence  of  secretion.  The  nature  of  such  a  cause  of  asthma  has  been 
the  subject  of  much  speculation. 

Traube1  regarded  a  catarrhus  acutissimus  of  the  finer  bronchi  as 
the  cause,  supporting  this  belief  by  its  frequent  onset  with  coryza. 
Some  clinical  confirmation  of  this  is  offered  by  Stork's2  observation 
of  strong  congestion  of  the  larynx  and  the  air  passages  even  to  the 
bronchi  during  an  attack.  In  explanation  of  the  swelling  of  the  mucous 
membrane,  Weber3  suggested  a  nervous  vasomotor  widening  of  the 
bloodvessels  in  the  lower  air  passages,  similar  to  a  sudden  and  transient 
swelling  of  the  nasal  mucous  membrane,  so  frequently  observed. 

The  peculiar  character  of  the  sputum  in  asthma  was  first  recognized 
by  v.  Leyden,4  who  regarded  the  elongated,  octohedral  crystals,  which 
he  discovered,  as  a  cause  of  reflex  bronchial  spasm,  a  view  which  Cursch- 
mann  contested  on  the  ground  that  asthmatic  attacks  occur  without 
crystals,  and  in  cases  of  asthma  in  which  crystals  are  found  their 
number  and  development  are  not  always  in  relation  to  the  intensity 
and  duration  of  the  attacks. 

Bronchiolitis  Exudativa. — Curschmann5  describes  an  independent 
disease  of  the  bronchioles,  bronchiolitis  exudativa,  with  a  distinctive 
clinical  picture,  as  a  frequent  cause  of  asthma.  The  disease  is 
almost  always  chronic,  seldom  subacute.  Intervals  of  freedom  or 
periods  of  severe  bronchitis  alternate  with  isolated  and  transient  or 
recurring  and  protracted  attacks  of  asthma.  Chronic  catarrh  and 
emphysema  are  frequent  complications.  The  onset  of  the  asthmatic 
attacks  is  less  sudden  than  in  essential  asthma,  but  is  preceded  by 
a  period  of  dyspnea  lasting  for  a  variable  length  of  time.  In  the 
intervals  of  freedom  there  may  be  a  slight  cough,  with  scanty  sputum, 
but  such  symptoms  are  usually  due  to  complications.  The  sputum 
is  diagnostic — whitish  gray,  transparent,  very  tough,  and  of  the  con- 
sistency of  white  of  egg.  The  amount  varies  from  a  few  teaspoonfuls 
to  a  half-liter  in  twenty-four  hours.  Among  the  small  flakes  or  masses 
in  suspension  are  the  peculiar  "spirals"  within  which  Charcot-Leyden 
crystals  are  found.  The  spirals  bear  a  direct  relation  in  number  to 
the  frequency  and  intensity  of  the  asthmatic  attacks.  They  are  expec- 
torated in  especially  large  numbers  after  the  cessation  of  the  attack. 
To  them  may  be  attributed  the  obstacle  to  the  entrance  into  and 
exit  of  air  from  the  lungs.   But  the  sudden  onset  and  cessation  of  asth- 

1  Ges.  Beitr.  z.  Path.  u.  Physiol.,  ii,  981;  hi,  360-617. 

2  Mittheilungen  iiber  Asthmabronchiale,  etc.,  Stuttgart,  1875. 

3  Tagebl.  d.  45  Natur-forsch.  Versamml.  zu  Leipzig,  1872,  p.  159. 

4  Zur  Kenntniss  des  Asthmabronchiale,  Vortrag  auf  d.  Rostocker  Naturforsch.  Ver- 
samml., 1871,  Tagebl.,  p.  24,  u.  Virchow's  Arch.,  Band  liv,  u.  Deut.  militararztl.  Zeit 
1886,  Heft  11. 

6  Ueber  Bronchiolitis  exudativa  u.  ihr.  Verhaltniss  zum  Asthma  nervosum,  Deut. 
Arch.  f.  klin.  Med.,  Band  xxxii,  p.  1-34. 


48  DISEASES  OF   THE  BRONCHI 

matic  dyspnea  can  hardly  be  ascribed  to  the  spirals,  and  in  explana- 
tion of  this  a  spasm  of  the  bronchial  muscles  must  be  assumed,  as  an 
accessory  factor,  and  probably  in  consequence  of  the  respiratory  efforts. 
The  presence  of  spirals  indicates  bronchiolitis  exudativa,  and  their 
presence  is  exceptional  without  asthmatic  attacks.  If  the  extent  of  the 
process  is  slight  and  the  patient  insensitive,  asthmatic  attacks  may 
be  absent.  In  susceptible  individuals,  with  an  extensive  process,  asth- 
matic paroxysms  of  the  greatest  severity  are  most  certain  to  occur. 

The  observations  of  v.  Leyden  and  Curschmann  have  served  to 
emphasize  an  important  feature  of  asthma,  viz.,  the  almost  con- 
stant occurrence  of  a  peculiar  and  almost  distinctive  expectoration. 
Though  Curschmann's  spirals  may  contribute  to  the  dyspnea,  from  the 
mechanical  obstruction  which  they  offer  to  respiration,  they  cannot 
be  regarded  as  bearing  an  etiologic  relation  with  the  disease.  They 
are  probably  secondary,  and  arise  from  mechanical  conditions  in  the 
bronchioles. 

3.  Spasm  of  the  Diaphragm. — Wintrich1  and  Bamberger,-'  among 
others,  regarded  a  tonic  spasm  of  the  diaphragm  as  the  cause  of 
asthma.  This  would  explain  the  inflation  of  the  lungs  and  the  low 
position  of  the  diaphragm,  but  it  does  not  account  for  the  prolonged 
expiration,  the  bronchial  rales,  and  the  presence  of  a  peculiar 
sputum. 

4.  The  Nervous  System  as  a  Factor. — The  subjects  of  asthma  often 
present  what  for  want  of  a  better  term  has  been  spoken  of  as  a  neuro- 
pathic constitution.  In  some  instances  a  consideration  of  the  family 
history  and  attendant  manifestations  has  suggested  a  special  predispo- 
sition to  nervous  instability,  and  it  has  been  assumed  that  in  such 
individuals  causes  so  slight  as  to  be  otherwise  ineffective  are  capable 
of  giving  rise  to  asthmatic  attacks.  Thus  irritation  of  the  nasal  mucous 
membrane  or  such  psychic  factors  as  fright  or  emotion  may  start 
an  attack.  In  estimating  the  importance  of  the  nervous  system  it 
should  be  remembered  that  the  so-called  neuropathic  constitution 
may  as  well  be  regarded  a  consequence  as  a  cause  of  asthma. 

5.  Bronchial  Asthma  as  a  Phenomenon  of  Anaphylaxis. — The  clinical 
features  of  bronchial  asthma  closely  resemble  hypersusceptibility  or 
anaphylaxis  experimentally  produced  in  animals  by  the  injection  of 
small  doses  of  alien  proteid,  as  noted  by  Meltzer.3  If,  for  example, 
a  guinea-pig  be  injected  subcutaneously  or  intraperitoneally  with  a 
small  dose  of  horse  serum,  and  again  be  given  1  c.c.  of  the  same  serum 
after  an  interval  of  at  least  twelve  to  fourteen  days,  the  animal  dies 
within  a  few  minutes  with  symptoms  of  respiratory  failure.  The  lungs 
become  greatly  distended  and  so  remain  even  after  removal  from  the 
body  after  death  of  the  animal.  This  pulmonary  inflation  has  been 
shown  by  Auer  and  Lewis  to  be  due  to  bronchostenosis  of  peripheral 

1  Virchow's  Pathologie,  1854,  vol.  v.  2  Wiirzh.  med.  Zeitsch.,  18G5,  Bd.  vi. 

3  Trans.  Assoc.  Amer.  Phys.,  1910,  xxv,  66. 


BRONCHIAL  ASTHMA  49 

origin,  which  probably  arises  in  consequence  of  tonic  contraction  of 
the  bronchial  muscles,  and  can  be  prevented  and  the  life  of  the  animal 
saved  by  a  previous  injection  of  atropin.  At  present  this  seems  the 
most  likely  explanation  of  bronchial  asthma.  Patients  with  this 
disease  may  have  become  sensitized  to  some  form  of  protein  by  absorp- 
tion from  the  alimentary  canal  into  the  circulation,  and  react  with  an 
attack  of  asthma  as  a  manifestation  of  subsequent  absorption  of  an 
intoxicating  dose  of  the  same  substance.  An  individual  sensitized 
in  some  way  to  pollen  dust  or  the  emanations  from  certain  animals  has 
an  anaphylactic  reaction  when  reexposed  to  the  specific  substance  to 
which  he  is  sensitized.  The  fact  that  hypersusceptibility  to  foreign 
proteid  may  be  transmitted  from  mother  to  offspring  in  animals  is 
a  further  point  of  resemblance,  as  the  disposition  to  asthma  may  be 
inherited  or  acquired.  The  influence  of  atropin  in  the  prevention 
of  the  anaphylactic  attack  in  animals  and  its  effect  in  relieving  bron- 
chial asthma  may  also  be  mentioned. 

Koessler1  has  reported  3  cases  in  which  attacks  of  bronchial  asthma 
could  be  traced  to  hen's  eggs.     Talbot2  has  reported  six  similar  cases. 

Conclusions. — Of  the  different  theories,  that  which  assumes  a  spasm 
of  the  diaphragm  may  be  set  aside  as  unlikely.  A  disturbance  in  the 
bronchial  mucous  membrane  accompanied  by  swelling  and  hypersecre- 
tion would  account  for  the  symptoms  of  the  disease.  A  coincident 
spasm  of  the  bronchial  muscles  cannot  be  excluded.  The  intimate 
association  of  the  mucous  membrane  and  the  bronchial  muscles  and 
their  common  nerve  supply  suggest  that  both  may  participate  as  the 
immediate  cause  of  the  paroxysm. 

Granted,  however,  that  the  immediate  cause  lies  in  the  bronchial 
mucous  membrane  or  the  bronchial  muscles  or  both,  some  underlying 
and  principal  factor  must  still  be  assumed  to  exist  in  explanation  of  the 
disturbance.  Whether  this  is  in  or  outside  the  individual  it  is  impos- 
sible to  say,  but  it  may  be  conjectured  that  both  external  and  internal 
influences  play  a  part  in  the  disease.  The  external  causes  apparently 
capable  of  initiating  a  paroxysm  in  susceptible  persons  are  so  variable 
as  naturally  to  suggest  that  an  important  determining  factor  lies 
within  the  individual  himself.  There  is  no  evidence  in  favor  of  a 
"neurosis"  as  the  cause.  Meltzer's  theory  that  asthma  is  an  anaphy- 
lactic phenomenon,  i.  e.,  that  asthmatics  are  individuals  who  are 
"sensitized"  to  a  specific  substance  and  the  attack  sets  in  whenever 
they  are  "intoxicated"  by  that  substance  seems  the  most  plausible 
explanation. 

Etiology. — This  is  unknown.  Many  of  the  predisposing  and  exciting 
factors  commonly  enumerated  can  be  established  in  so  small  a  propor- 
tion of  cases  as  to  make  their  actual  importance  doubtful. 

Predisposing  Factors. — Heredity. — This  appears  to  bear  some  rela- 
tion to  the  disease.    Thus  Salter3  observed  an  inherited  disposition 

1  Illinois  Med.  Jour.,  January,  1913. 

2  Bost.  Med.  and  Surg.  Jour.,  November  5,  1914.  3  On  Asthma,  London,  1850. 

4 


50  DISEASES  OF  THE  BRONCHI 

to  the  disease  in  14  of  35  cases.  Berkart1  noted  it  in  16  per  cent. 
Asthma  may  have  existed  in  the  parents  or  show  itself  in  the  patient's 
brothers  or  sisters.  Migraine,  neurasthenia,  hysteria,  epilepsy  or 
gout  may  occur  in  the  family  history.  Age:  No  age  is  exempt.  It  is 
not  infrequent  in  young  children  and  may  be  seen  in  infancy.  Of 
Salter's  225  cases,  in  31  per  cent,  the  asthma  began  before  the  age  of 
ten.  More  than  a  third  of  Berkart's  cases  were  under  ten  years  of 
age.  Of  105  patients  in  SokolowskiV  series,  65  were  forty  or  under. 
Sex:  Males  appear  to  be  more  frequently  affected;  67  of  Sokolowski's 
cases  were  males. 

The  Nose  and  Asthma. — Voltolini3  was  the  first  to  call  attention 
to  the  relation  between  diseases  of  the  nose  and  asthma.  He  obtained 
relief  of  asthma  by  the  removal  of  nasal  polypi.  Confirmatory  obser- 
vations have  been  made,  among  others  by  Hanisch,4  Schaffer,5  Porter,6 
Daly,7  B.  Frankel,8  Hach,9  Schmiegelow,10  and  Heyman.11  The  pro- 
portion of  cases  of  asthma  with  nasal  disease  may  be  gathered  from 
the  statistics  of  Francis,12  who  found  mucous  polypi  in  36  marked 
obstructive  lesions  in  27,  and  the  nasal  passages  apparently  free  in 
379  of  442  cases  of  asthma.  When  the  frequency  of  such  nasal  lesions 
in  patients  at  large  is  considered  this  is  not  a  very  striking  proportion. 
On  the  other  hand,  patients  with  nasal  disease  only  occasionally  have 
asthma.  .In  Schmiegelow's13 139  cases  with  nasal  polypi,  31  had  asthma, 
and  of  514  patients  with  chronic  rhinitis,  40  had  asthma.  The  propor- 
tion was  even  smaller  in  Bocker's14  series.  Of  310  cases  of  nasal  polypi 
only  9  had  asthma.  It  is  sufficiently  obvious,  therefore,  that  asthma 
is  not  always  due  to  nasal  disease  and  that  nasal  disease  is  more  often 
unaccompanied  by  asthma  than  the  contrary.  The  relation  of  nasal 
disease  to  asthma,  however,  cannot  be  thus  lightly  dismissed.  To 
be  sure  the  results  of  treatment  of  the  nose  in  asthmatics  with  nasal 
disease  is  often  unsuccessful  in  relieving  the  asthma.  Thus  Sokolowski, 
after  various  operations  in  more  than  20  patients,  obtained  a  favorable 
and  permanent  result  in  only  1,  an  improvement  for  two  months  in  a 
second,  and  negative  results  in  the  remaining  cases.  But  even  an 
occasional  success  justifies  the  belief  in  a  possible  relation  between 
nasal  disease  and  asthma,  at  least  in  certain  individuals  whose  nasal 
mucous  membrane  may  be  especially  sensitive,  or  in  whom  the  nasal 
lesions  are  so  situated  as  to  implicate  a  particular  region  in  the  nose. 
Brodie  and  Dixon's  finding  that  stimulation  of  the  upper  and  posterior 

1  On  Bronchial  Asthma,  its  Pathology  and  Treatment,  London,  1889,  2d  ed.,  pp.  81 
to  89. 

2  Klinik  dcr  Brustkrankheiten,  1906,  1. 

3  Anwendung  der  Galvanokaustik  im  Innern  des  Kehlkopfes,  1872,  2  Aufl. 
*  Berlin  klin.  Woch.,  1874.  <■  Deut.  med.  Woch.,  1879. 

6  New  York  Med.  Record,  1879.  7  Trans.  Amer.  Laryng.  Assoc,  1881. 

s  Berlin  klin.  Woch.,  1881.  9  Wein.  med.  Woch.,  1882-83. 

1(1  Stagerng's  "Forlag,"  Copenhagen,  1889.     u  Deut.  med.  Woch.,  1886. 

12  Asthma  in  Relation  to  the  Nose,  London,  1903. 

13  Asthma  Considered  Specially  in  Relation  to  Nasal  Disease,  London. 
»  Deut.  med.  Woch.,  1886,  Nos.  26  and  27. 


BRONCHIAL  ASTHMA  51 

part  of  the  nasal  septum  caused  a  reflex  contraction  of  the  bronchial 
muscles  in  animals  should  not  be  forgotten.  Francis  claims  to  have 
cured  over  300  cases  of  asthma  by  cauterizing  the  nasal  septum. 
He  regards  that  part  of  the  septum  which  lies  opposite  and  immediately 
above  the  anterior  third  of  the  middle  turbinate  body  as  the  most 
satisfactory  spot  to  cauterize. 

Some  relation  has  been  thought  to  exist  between  asthma  and  such 
diseases  as  rickets,  scrofulosis,  hysteria,  neurasthenia,  gout,  urticaria, 
and  psoriasis.  It  is  believed  to  be  more  common  among  the  well-to-do. 
No  constant  relation  has  been  established  between  renal  or  pulmonary 
disease  and  asthma.  It  is  said,  however,  that  asthmatics  rarely  become 
tuberculous  and  that  tuberculous  patients  seldom  suffer  from  asthma. 
An  explanation  of  the  paroxysms  has  been  sought  in  a  reflex  from  such 
organs  as  the  stomach,  intestines,  ear,  teeth,  skin  and  genitals,  but 
without  much  justification. 

Exciting  Causes. — Much  variation  is  noted  in  different  patients 
in  respect  to  the  influence  of  the  season,  but  in  general  the  disease 
is  more  prevalent  from  spring  to  autumn.  No  definite  and  constant 
influence  can  be  ascribed  to  geographic  factors.  In  some  patients, 
attacks  may  be  induced  or  aggravated  by  residence  in  a  dry  climate. 
Others  seem  equally  susceptible  to  moist  regions.  Some  are  subject 
to  asthma  in  the  city,  other  in  the  country,  or  in  special  localities  only. 
Of  the  many  and  various  exciting  causes,  among  others  may  be  men- 
tioned such  psychic  influences  as  excitement,  fright,  anxiety,  and 
even  autosuggestion  from  "the  fragrance  of  an  artificial  rose."  An 
almost  indefinite  number  of  causes  capable  of  exciting  an  attack  in 
susceptible  individuals  might  be  mentioned.  Exposure  to  pollen  dust 
coal  dust,  or  wood  dust,  to  ipecacuanha,  resin,  coffee,  or  sulphur,  the 
odor  of  freshly  mowed  fields,  of  violets  or  roses,  even  the  emanations 
from  animals  (horse,  dog,  or  cat)  or  from  certain  persons  may  be 
sufficient  to  induce  a  paroxysm.  Attacks  have  been  noted  when  the 
wind  shifts  to  a  certain  quarter.  They  may  occur  only  during 
pregnancy  or  at  the  menopause. 

Pathology. — The  opportunity  to  make  postmortem  examinations 
on  patients  who  have  died  during  an  attack  of  asthma  is  seldom  offered. 
Cases  have  been  reported  by  von  Leyden1,  Berkart,2  Schmidt,3  Frankel,4 
Jezierski,5  and  by  Ellis,6  who  has  reviewed  the  literature.  The  patho- 
logic picture  is  not  uniform  or  characteristic  of  asthma.  Redness 
of  the  bronchial  mucosa,  dilatation  of  the  bronchi,  and  pulmonary 
emphysema  are  common.  The  medium  and  smaller  bronchi  are  likely 
to  be  wholly  or  partially  occluded  by  an  exudate  of  mucus,  which 
may  contain  a  granular  or  apparently  fibrinous  material,  and  intact 

1  Deut,  militararztl.  Zeit.,  1886,  Heft  2.  2  On  Bronchial  Asthma,  1889,  2d  ed. 

3  Zeit.  f.  klin.  Med.,  1892,  Bd.  xx,  p.  476. 

4  Ibid.,  1898,  Bd.  xxxv,  p.  559,  and  Deut.  med.  Woch.,  1900,  No.  17,  p.  269. 

5  Deut.  Arch.  f.  klin.  Med.,  1905,  Bd.  lxxxv,  p.  342. 

6  Amer.  Jour.  Med.  Sci.,  September,  1908. 


52  DISEASES  OF  THE  BRONCHI 

or  degenerated  epithelium.  Partly  wound  threads  or  spirals  may  also 
be  observed.  Polynuclear  leukocytes,  round,  oval,  or  spindle  cells, 
with  or  without  eosinophils  and  Charcot-Leyden  crj'stals,  may  also 
be  present.  The  epithelium  of  the  bronchial  mucosa  may  be  intact 
or  desquamated.  The  bronchial  wall  itself  may  be  unchanged.  It 
may  show  hyperemia  or  even  small  hemorrhages,  or  thickening  and 
infiltration  with  round  cells.  Eosinophils  may  be  present.  Charcot- 
Leyden  crystals  have  been  found  in  the  bronchial  wall.  The  elastic 
tissue  may  be  increased.  The  pulmonary  alveoli  may  appear  normal, 
dilated,  or  atelectatic.  Eosinophile  cells  were  noted  in  the  alveoli  of 
Ellis'  case. 

Symptoms. — The  asthmatic  attack  may  be  preceded  by  very  variable 
premonitory  symptoms.  These  may  be  catarrhal  and  such  as  accom- 
pany a  cold,  chilliness,  coryza,  conjunctival  injection,  lacrimation, 
nasal  occlusion,  sneezing,  and  laryngeal  irritation,  which  gives  rise 
to  cough.  In  other  cases  the  patient  is  warned  of  an  approaching 
paroxysm  by  substernal  oppression  or  an  indefinable  general  feeling 
of  malaise.  Some  patients  are  depressed;  others  experience  a  feeling 
of  special  well-being  just  before  the  attack.  There  may  be  epigastric 
discomfort  or  flatus.  The  passage  of  a  large  amount  of  urine  may 
usher  in  an  attack.  In  children  the  attacks  are  specially  likely  to  be 
preceded  by  bronchitis  and  initiated  by  catarrhal  symptoms.  In  a 
considerable  proportion  of  the  cases  the  paroxysm  occurs  without 
previous  warning. 

The  Attack.— The  onset  is  almost  always  sudden.  It  may  come  on 
at  any  time,  but  is  most  likely  to  occur  at  night,  after  a  few  hours  of 
sleep.  The  frequent  nocturnal  onset  is  difficult  to  explain.  It  may  be 
due  to  the  influence  on  a  hypersensitive  respiratory  mucous  membrane 
of  secretion  accumulated  during  sleep.  The  patient  is  aroused  by  a 
distressing  sense  of  oppression  and  want  of  breath,  which  rapidly 
increases  to  extreme  dyspnea.  There  is  a  short,  dry  cough,  at  first 
without  expectoration.  As  the  intensity  of  the  paroxysm  increases 
the  patient  may  become  greatly  alarmed  for  fear  of  suffocation.  He 
sits  up  or  leaves  the  bed  and  seeks,  very  likely  in  vain,  to  assume  a  more 
favorable  position,  sitting,  half  supported  by  his  arms,  upright  with 
his  hands  beside  him,  bent  forward  with  his  elbows  on  his  knees  or  the 
arms  of  a  chair  or  backward  with  arms  outstretched.  He  may  rush 
to  the  open  window.  The  face  may  be  pale,  its  expression  anxious 
and  speech  difficult  or  impossible.  In  spite  of  the  most  strenuous 
inspiratory  efforts,  in  which  all  the  accessory  respiratory  muscles  are 
brought  into  play,  very  little  air  enters  or  leaves  the  lungs.  The 
expiration  is  prolonged.  In  severe  attacks,  both  phases  of  respiration, 
especially  expiration,  may  be  accompanied  by  loud  wheezing,  audible 
even  at  a  distance  from  the  patient.  With  the  continuance  of  the  attack 
signs  of  defective  aeration  are  manifest.  The  patient  becomes  cyanotic, 
a  cold  sweat  breaks  out,  especially  on  the  face,  and  the  extremities  are 
cold  and  clammy. 


BRONCHIAL  ASTHMA  53 

The  paroxysm  may  last  from  a  few  minutes  to  several  hours. 
Improvement  is  likely  to  be  gradual.  During  the  course  of  the  attack 
the  cough  increases  and  the  expectoration  of  tenacious  mucus  becomes 
easier  and  more  abundant.  The  patient,  exhausted  by  his  efforts,  may 
fall  asleep,  perhaps  to  be  again  interrupted  on  the  same  or  another  night. 

Physical  Signs. — During  the  attack,  owing  to  the  excessive  respira- 
tory efforts  and  deficient  expiration,  the  amount  of  residual  air  in  the 
thorax  is  increased  and  the  lungs  abnormally  inflated.  On  inspection 
the  distended  thorax  and  the  lack  of  thoracic  motion,  even  with  the 
most  strenuous  respiratory  efforts,  are  striking  features.  The  breathing 
is  costal  in  type.  The  diaphragm  is  low  and  its  excursion,  as  indicated 
by  the  diaphragm  shadow,  is  diminished  or  absent.  The  abdominal 
muscles  actively  participate  in  the  expiratory  effort  and  are  firmly 
contracted.  Inspiration  is  quick  and  shallow.  Expiration  is  much 
prolonged.  The  rate  of  respiration  is  unchanged  or  diminished  from 
the  prolongation  of  expiration. 

On  percussion  no  abnormality  may  be  noted  in  the  character  of  the 
sound.  If  the  patient  has  long  been  the  subject  of  asthma  it  is  likely 
to  be  hyperresonant.  It  may  have  a  tympanitic  quality — Biermer's 
"box  tone."  On  percussing  the  pulmonary  boundaries  their  lower 
limits  are  usually  found  to  be  abnormally  low  and  their  downward 
excursion  with  inspiration  limited  in  extent.  The  pulmonary  disten- 
tion may  diminish  or  even  obliterate  the  superficial  cardiac  dulness. 
The  hepatic  dulness  may  be  greatly  depressed. 

On  auscultation  the  inspiration  is  weak,  the  expiration  abnormally 
loud  and  long.  Both  inspiration  and  expiration  may  be  inaudible 
from  the  presence  of  numerous  sibilant  and  sonorous  rales  which  are 
very  variable  in  their  character,  high  or  low  pitched,  loud  or  soft, 
and  long  or  short.  Toward  the  end  of  the  attack  there  may  be  numer- 
ous moist  rales.  The  pulse  may  be  elevated  during  the  attack.  The 
temperature  is  normal  in  the  absence  of  complications. 

Sputum. — There  is  usually  no  expectoration  until  toward  the  end 
of  the  attack.  In  uncomplicated  cases  the  sputum  is  distinctive  of 
bronchial  asthma.  It  is  often  raised  only  with  great  effort,  and  con- 
sists of  small,  rounded,  sago-like  balls,  mixed  with  a  small  amount  of 
thin  mucus.  These  small  masses  are  more  or  less  translucent,  grayish 
white  to  yellowish  green  in  color,  and  very  tenacious.  They  are  the 
so-called  "perles"  of  Laennec.  The  expectoration  usually  continues 
for  several  days  after  the  cessation  of  the  paroxysm. 

Curschmann  Spirals. — Examination  of  the  finer  structure  of  the 
specimens  is  best  conducted  on  a  black  background.  Some  of  these 
pellets  can  be  unfolded  into  elongated  masses  in  which  with  the  naked 
eye  a  twisted,  cork-screw-like  character  can  be  demonstrated.  They 
are  the  so-called  "spirals."  It  is  indeed  surprising  that  such  peculiar 
structures  should  have  been  overlooked  until  Curschmann's  descrip- 
tion in  1883.1    They  vary  greatly  in  size,  but  are  approximately  from 

1  Deut.  Arch.  f.  klin.  Med.,  1883,  vol.  xxxii. 


54 


DISI-ASES   OF   THE   Bh'OXCIIl 


I)..")  to  1  mm.  in  diameter  and  2  or  more  cm.  long.  Under  the  low  power 
of  the  microscope  they  are  seen  to  be  composed  of  a  variable  number 
of  coarse  or  fine  threads  loosely  or  tightly  twisted  into  cork-screw- 
shaped  structures,  in  some  of  which  an  interruption  of  the  circular 
winding  may  give  place  to  a  bundle  of  straight  or  curved,  divergent 
or  convergent  fibers.  Within  the  substance  of  the  spirals,  higher 
powers  of  the  microscope  usually  disclose  large  numbers  of  round 
cells,  the  majority  of  which  from  their  coarse  granulations  or  after 
appropriate  staining  can  be  recognized  as  eosinophils,  with  spindle- 
shaped  cells  in  smaller  proportion.  Within  some  of  the  spirals  only 
a  granular  detritus  is  found.  Charcot-Leyden  crystals  are  almost 
constant. 

Fig.  S 


$&&*> 


Curschmann's  spirals.     (Curschmann.) 


The  spirals  often  present  a  still  more  interesting  and  peculiar 
structure.  There  may  often  be  found,  within  the  centre  and  axially 
placed,  a  delicate,  sharply  outlined,  extraordinarily  clear  and  trans- 
lucent filament,  the  "central  thread."  Under  the  low  power  of  the 
microscope  it  appears  single  and  homogeneous.  With  higher  magni- 
fication it  is  usually  found  to  be  made  up  of  the  most  delicate,  closely 
twisted,  separate  filaments,  which  may,  however,  in  places  be  partly 
unwound.  In  rare  instances  the  central  thread  is  apparently  actually 
single  and  cannot  thus  be  resolved  into  associated,  individual  filaments. 

Much  variation  in  the  structure  of  the  spirals  is  common.  As  well 
as  typical  spirals,  with  and  without  central  threads,  there  may  be 
isolated  single  filaments  or  central  threads,  about  which  only  one  or 
more  delicate  threads  are  spirally  twisted.  In  some  instances  the 
spirals  may  be  hollow7  and  air-holding,  cylindrical,  or  even  nearly 
spherical  in  shape.  In  cases  complicated  with  bronchitis  and  an  abun- 
dant excretion,  they  may  be  readily  overlooked  unless  the  specimens 


BRONCHIAL  ASTHMA  55 

of  sputum  are  carefully  examined.  Riehl1  has  made  the  unusual 
observation  in  four  patients  of  "giant"  spirals,  ranging  from  6  to  24 
cm.  long,  and  at  times  reaching  a  diameter  of  3  to  3.5  cm.  and  without 
spirals  of  the  ordinary  size. 

Curschmann's  spirals  are  found  with  greater  frequency  and  in  larger 
numbers  in  the  sputum  of  bronchial  asthma  than  in  other  conditions, 
but  they  are  not  peculiar  to  asthma.2 

The  exact  nature  of  the  spiral  filaments  is  uncertain.  Frankel3 
believes  them  in  part  to  be  elongated  ciliated  epithelium.  The  denser 
central  threads  are  probably  of  the  same  nature  as  the  encircling 
filaments.  Spirals  with  central  threads  may  be  artificially  made  by 
spirally  twisting  mucus  from  the  sputum  of  various  pulmonary  con- 
ditions. In  explanation  of  their  formation,  Osier  offers  the  suggestion 
that  the  course  of  the  currents  produced  by  the  ciliated  epithelium 
may  be  rotatory,  and  that  this,  in  combination  with  spasm  of  the 
bronchial  muscles,  may  twist  the  mucus  formed  in  the  tube  into  a 
spiral  form. 

Charcot-Leyden  Crystals. — These  were  first  described  by  Charcot 
and  Robin4  at  autopsy  in  the  blood,  spleen,  and  liver  of  patients  with 
leukemia.  Since  Charcot  and  Vulpian's5  description  they  have  usually 
been  regarded  as  elongated  octohedra.  Von  Leyden6  first  noted  their 
almost  constant  presence  in  asthmatic  sputum  and  demonstrated 
them  in  six  of  seven  cases.  Curschmann7  found  them  constantly 
absent  in  only  4  of  38  cases.  It  may  be  necessary  to  let  the  sputum 
stand  for  a  time  to  demonstrate  them.  Their  presence  may  be  indi- 
cated by  a  gritty  resistance  between  cover-glass  and  slide.  The 
crystals  are  present  during  the  paroxysms,  absent  in  the  remissions. 
They  are  most  abundant  in  and  about  the  spirals,  throughout  the 
length  of  which  they  may  be  equally  or  unequally  distributed,  but 
at  times  demonstrable  in  the  more  fluid  parts  of  the  specimens.  A 
later  and  more  careful  study  of  their  shape  by  Th.  Cohn8  indicates  that 
they  are  hexagonal  rather  than  octahedral  crystals,  appearing  as  very 
delicate,  elongated  and  sharply  pointed,  double  pyramids.  They  are 
colorless,  of  a  dull  luster,  and  vary  in  size  from  those  visible  only  with 
the  highest  magnification  up  to  0.075  mm.  long  and  0.04  mm.  wide, 
with  an  apical  angle  of  from  17  to  20  degrees. 

1  Munch,  med.  Woch.,  1906,  No.  46,  p.  2240,  and  No.  47,  p.  2302. 

2  Curschmann  spirals  have  also  been  found  in  pneumonia  by  Vierordt  (Berl.  klin. 
Woch.,  1883,  No.  29),  v.  Jaksch  (Centralb.  f.  klin.  Med.,  1883,  No.  31,  p.  417),  Pel 
(Zeit.  f.  klin.  Med.,  Bd.  ix,  pp.  29  to  52),  Patella  (Annali  universali  di  medicina,  1884, 
vol.  cclxvii),  Curschmann  (Deut.  Arch.  f.  klin.  Med.,  Bd.  xxxvi,  pp.  578  to  585)  and 
Predtetschensky  (Zeit.  f.  klin.  Med.,  1906,  lix,  29).  Kaufmann  (Lehrbuch  der  spez. 
Path.  Anat.,  1907,  Auf.  4,  p.  204)  repeatedly  found  them  in  the  tough  mucus  behind 
bronchial  stenosis  due  to  anthracotic  bronchial  lymph  nodes  or  primary  and  secondary 
tumors  of  the  bronchial  wall. 

3  Spez.  Path.  u.  Ther.  d.  Lungenkrankheiten,  1904,  p.  90. 

4  Comp.-rend.  de  la  Soc.  de  Biol.,  1853,  p.  47. 

5  Gaz.  hebd.,  1860,  vii,  47.  6  Virchow's  Arch.,  1872,  vol.  liv. 
'  Deut.  Arch.  f.  klin.  Med.,  1883,  vol.  xxxii.  8  Ibid.,  1895,  vol.  liv. 


56  DISEASES  OF   THE  BRONCHI 

Owing  to  the  difficulty  of  isolating  the  crystals  from  the  medium 
in  which  they  are  found,  their  chemical  properties  are  uncertain,  but 
tested  microchemically,  Th.  Cohn  found  them  insoluble  in  cold  water, 
ether,  alcohol,  xylol,  chloroform,  creosote,  and  iodin  solution;  soluble 

Fig.  9 


Charcot-Leyden  crystals,     (v.  Leyden.) 


in  warm  water,  hydrochloric  acid,  nitric  acid,  sulphuric  acid,  phos- 
phoric acid,  acetic  acid,  oxalic  acid,  picric  acid,  and  carbolic  acid, 
potassium  and  sodium  hydrate,  and  ammonia. 

The  crystals  are  not  peculiar  to  asthma,  but  are  present  in  a  great 
variety  of  other  conditions.1 

1  The  crystals  have  been  demonstrated  after  death  in  the  blood  and  tissues  of  leu- 
kemic patients  by  Charcot  and  Robin  (loc.  cit.),  Charcot  and  Vulpian  (loc.  cit.),  Neu- 
mann (Arch.  f.  mik.  Anat.,  1866,  Band  ii,  p.  507),  Eberth  (Virchow's  Arch.,  1868), 
Lauenstein  (Deut.  Arch.  f.  klin.  Med.,  1876,  Band  xviii,  p.  120),  Zenker  (ibid.,  p.  125), 
and  others;  in  blood  from  living  patients  with  leukemia  by  Prus  (Warschauer  med. 
Zeit.,  "Medecyna,"  1886,  Nos.  39  and  40);  in  material  obtained  by  puncture  of  the 
leukemic  spleen  by  Westphal  (Deut.  Arch.  f.  klin.  Med.,  1890-91,  47) ;  in  ordinary  bron- 
chitis by  Bizzozero  (Handbuch  der  klinischen  Mikroscopie,  1863,  p.  215) ;  in  tubercu- 
lous sputum  by  Meissen  (Berl.  klin.  Woch.,  1883,  No.  22);  in  the  feces  of  patients 
with  helminthiasis  by  Baumler  (Correspondenzbl.  f.  Schweizer  Aerzte,  1881,  No.  19); 
Nothnagel  (Zeit.  f.  klin.  Med.,  Band  iii,  p.  352),  and  Leichtenstern  (Deut.  med.  Woch., 
1892,  No.  25) ;  in  normal  bone  marrow  after  death  by  Neumann  (loc.  cit.) ;  in  nasal  polypi 
and  cancer  of  the  cervix  uteri  by  B.  Lewy  (Zeit.  f.  klin.  Med.,  1900,  40) ;  and  the  pus  from 
pleural  empyema  by  Eichhorst  (Handbuch  der  spec.  Path.  u.  Ther.,  4  Aufl.,  i,  p.  550). 

The  identity  of  Bottcher's  sperm-crystals  and  Lubarsch's  testicular  epithelium  crys- 
tals with  Charcot-Leyden  crystals  is  doubted  by  Th.  Cohn  (loc.  cit.,  and  Centralb.  f. 
allg.  Path.  u.  path.  Anat.,  1899,  Band  x,  p.  940). 

Von  Noorden  (Zeit.  f.  klin.  Med.,  1892,  Band  xx,  pp.  98-106)  specially  called  attention 
to  the  presence  within  the  leukocytes  and  alveolar  epithelium  of  yellow  and  brown 
pigment,  which  he  regarded  from  its  microchemical  reactions  as  hemosiderin  and 
probably  due  to  small  hemorrhages. 


BRONCHIAL  ASTHMA 


57 


The  origin  of  the  Charcot-Leyden  crystals  is  unknown.  The  close 
association  of  eosinophils  and  Charcot-Leyden  crystals,  in  number 
and  distribution,  not  only  in  the  sputum  of  bronchial  asthma  but  under 
other  conditions,  suggests  a  possible  relation  between  them. 

Von  Leyden  was  disposed  to  regard  the  crystals  as  a  cause  of  the 
asthmatic  paroxysm,  from  irritation  of  the  bronchial  mucous  mem- 
brane and  the  terminations  of  the  vagus,  with  consequent  reflex 
spasm  of  the  bronchial  muscles.  It  is  more  likely  that  they  are  sec- 
ondary to  degenerative  processes  in  the  sputum,  a  view  which  receives 
some  confirmation  from  Ungar's1  experimental  formation  of  crystals 
in  sputum  preserved  in  a  moist  chamber. 


Fig.  10 


Asthma  sputum.     Four  eosinophiles  and  one  polynu clear  leukocyte. 

Eosinophiles. — The  numerous  large  granular  cells  and  intercellular 
granules  noted  by  v.  Leyden  in  the  small  masses  of  sputum  from 
patients  with  asthma  were  probably  eosinophiles  and  their  fragments. 
The  identity  of  such  cells  with  the  eosinophiles  of  the  blood  and  their 
increase  in  asthmatic  sputum  were  shown  by  Fr.  Miiller,  Gollasch,2 
Fink,3  and  others.  They  may  be  found  in  small  numbers  in  the  sputum 
of  patients  with  various  pulmonary  conditions.  They  are  often  very 
numerous  in  the  sputum  from  cases  of  bronchial  asthma,  and  may 
outnumber  other  cells  in  the  specimens.  In  Fink's  case  they  amounted 
to  from  20  to  90  per  cent,  of  the  cells  in  the  sputum;  in  Aronson  and 
Philip's4  case  to  nearly  two-thirds.  Both  mononuclear  and  poly- 
nuclear  types  are  found,  but  mononuclears  are  more  common.  They 
are  most  numerous  in  and  about  the  spirals. 

1  Centralbl.  f.  klin.  Med.,  1880,  No.  40. 

2  Fortschritte  der  Med.,  1889,  No.  7,  p.  361. 

3  Beitrage  z.  Kenntniss  des  Eiters  und  des  Spu turns,  Diss.,  Elberfeld,  1S90. 

4  Deut.  med.  Woch.,  1892,  No.  3,  p.  48. 


58  DISEASES  OF   THE  BRONCHI 

An  increase  of  eosinophils  in  the  bronchial  secretion  is  usually 
associated  with  an  eosinophilia  also  in  the  circulating  blood.  This  is 
not  constantly  present,  and  when  it  occurs  is  usually  confined  to 
the  period  of  the  attack,  as  in  the  cases  reported  by  Neusser,1 
Mandybur,2  v.  Noorden,3  and  Fink.4  The  differential  counts  often 
show  from  10  to  20  per  cent,  eosinophiles.  In  Billing's  case5  they 
reached  the  unusual  proportion  of  53.0  per  cent.,  in  Herrick's6  72.5 
per  cent.  Although  the  increase  in  eosinophiles  is  usually  confined  to 
the  period  of  the  attack  and  a  short  time  after  it,  it  may  be  persistent. 
In  Zappert's  case7  there  were  8.77  and  12.30  per  cent,  during  intervals 
of  freedom,  and  Wolff8  observed  a  case  for  over  a  year,  during  six 
months  of  which  the  patient  was  free  from  asthmatic  attacks,  and  yet 
the  blood  constantly  showed  about  10  per  cent,  of  eosinophiles,  with- 
out increase  during  the  paroxysms. 

It  is  uncertain  whether  the  eosinophiles  are  formed  locally  in  the 
bronchial  tissue  or  in  other  organs  and  carried  thence  to  the  bronchi. 

Course  and  Complications. — The  severity  of  the  attacks  varies 
greatly.  Their  frequency  likewise  is  subject  to  much  variation  in  the 
same  or  in  different  patients.  There  may  be  a  daily  repetition  of  one  or 
more  attacks.  Successive  attacks  over  a  period  of  days  or  weeks,  in 
the  intervals  between  which  the  patient  coughs  and  is  short  of  breath, 
are  frequent.  The  paroxysms  may  occur  singly,  with  long  intervals 
of  freedom.  Recurrences  may  be  limited  to  one  season  of  the  year 
or  occur  only  after  exposure  to  certain  exciting  causes  already 
mentioned. 

If  the  attacks  are  frequently  repeated  and  severe,  a  cough  and  some 
shortness  of  breath  is  likely  to  persist  between  the  paroxysms.  The 
sputum,  both  during  the  attacks  and  in  the  intervals  of  freedom, 
gradually  becomes  more  abundant,  and  changes  from  its  more  typical 
mucous  character  to  mucopurulent  and  finally  becomes  purulent. 
The  clinical  features  are  now  those  of  chronic  bronchitis,  to  which 
bronchiectasis  and  emphysema  may  be  added.  As  the  pulmonary 
embarrassment  increases,  and  usually  after  the  disease  has  lasted  for 
years,-  hypertrophy  of  the  heart  may  be  demonstrated.  Signs  of 
cardiac  insufficiency  finally  ensue.  Under  the  burden  of  such  compli- 
cations, the  patient  becomes  more  and  more  an  invalid.  Such  severe 
cases  are  likely  to  be  fatally  interrupted  by  an  acute  bronchopneu- 
monia or  cardiac  dilatation. 

Diagnosis. — This  is  usually  easily  made.  It  may  be  sufficiently 
obvious  from  the  history.  The  sudden  onset  of  dyspnea  affecting  both 
phases  of  respiration,  but  especially  expiration,  the  cough,  the  peculiar 
expectoration,  the  distended  thorax,  and  the  sibilant  and  sonorous 

1  Wiener  klin.  Woch.,  1892,  Nos.  3  and  4.  2  Ibid.,  Nos.  7,  8,  9. 

3  Zeit.  f.  klin.  Med.,  Bd.  xx.  4  Loc.  cit. 

5  New  York  Med.  Jour.,  May  22,  1897. 

6  Jour.  Amer.  Med.  Assoc.,  December  2,  1911. 

7  Zeit.  f.  klin.  Med.,  1893,  Bd.  xxiii,  p.  227. 

8  Beitrage  z.  path.  Anat.  u.  allg.  Path.,  1900,  vol.  xxviii. 


BRONCHIAL  ASTHMA  59 

rales  are  typical  features.  An  eosinophilia  in  the  sputum  and  the  sys- 
temic blood,  if  present,  may  confirm  an  otherwise  doubtful  diagnosis. 
Curschmann's  spirals  and  Oharcot-Leyden  crystals  are  of  less  diag- 
nostic value. 

Attacks  of  paroxysmal  dyspnea,  like  those  in  essential  asthma, 
may  develop  in  the  course  of  chronic  bronchitis  and  emphysema. 
They  are  not  very  uncommon  in  such  cases,  and  are  probably  due 
to  spasmodic  contraction  of  the  bronchial  muscles  from  irritation  of 
the  bronchial  mucosa. 

Capillary  bronchitis  of  sudden  onset,  with  constant  cough,  extreme 
dyspnea,  marked  cyanosis,  and  sibilant  and  sonorous  rales,  may  occur 
in  infants  and  children  and  closely  simulate  asthma.  An  initial  chill, 
if  present,  and  fever  may  serve  to  differentiate  this  disease;  but 
there  are  cases  in  which  the  diagnosis  may  remain  in  doubt,  and  asthma 
may  be  excluded  only  by  the  subsequent  course  and  the  absence  of 
recurrent  attacks. 

First  attacks  of  asthma  must  be  differentiated  also  from  paroxysms 
of  dyspnea  which  arise  in  consequence  of  obstruction  in  the  upper  part 
of  the  respiratory  tract.  Such  obstruction  is  most  common  in  the 
larynx  or  trachea.  It  may  be  due  to  pressure  from  without,  as  by 
enlarged  glands,  mediastinal  tumors,  goitre,  or  aortic  aneurysm; 
the  lodgement  of  foreign  bodies  in  the  pharynx,  larynx,  or  trachea; 
inflammatory  swelling  of  the  larynx,  as  in  croupous  or  subglottic 
laryngitis;  edematous  laryngitis;  spasmodic  laryngitis  (laryngitis 
stridulus,  thymic  asthma),  and  paralysis  of  the  adductors.  In  all 
these  conditions  the  dyspnea  is  predominantly  inspiratory,  while  it 
is  more  markedly  expiratory  in  bronchial  asthma.  Inspiration  is 
also  likely  to  be  accompanied  by  stridor.  Such  an  accentuation  of  the 
inspiratory  phase  is  to  be  ascribed  to  the  greater  velocity  with  which 
the  inspired  air  must  pass  through  the  obstruction.  When  the  larynx 
is  involved  there  is  likely  to  be  hoarseness  or  even  aphonia.  In  conse- 
quence of  the  increased  negative  pressure  within  the  thorax  during 
the  labored  inspiration  the  epigastrium,  the  lower  lateral  thoracic 
regions,  the  intercostal  spaces,  the  suprasternal  notch,  and  the  supra- 
clavicular and  infraclavicular  fossae  are  depressed;  the  trachea  and 
with  it  the  larynx  are  forced  downward.  The  history,  the  attendant 
symptoms,  the  character  of  the  breathing,  the  change  in  or  loss  of  the 
voice,  and  the  laryngoscopic  picture  will  usually  serve  to  differentiate 
these  conditions  from  asthma.  It  may  rarely  happen  that  a  sub- 
glottic polyp  with  a  long  pedicle  or  a  piece  of  freely  movable  membrane 
may  give  rise  to  expiratory  dyspnea,  by  partially  occluding  the  glottis 
during  expiration.  Inspiration  may  then  be  relatively  free,  as  the 
obstruction  falls  back  against  the  tracheal  wall  during  the  inflow  of 
air.  The  various  types  of  dyspnea,  arising  as  a  consequence  of  hysteria 
or  from  disease  of  the  medulla,  are  easily  distinguished  from  asthma. 

The  sudden  onset  of  dyspnea,  embarrassing  both  phases  of  respira- 
tion, may  occur  as  a  symptom  of  cardiac  disease  and  simulate  true 


GO  DISEASES  OF   THE  BRONCHI 

asthma,  the  so-called  cardiac  asthma.  Asthmatic  paroxysms  beginning 
in  persons  past  middle  life  arc  more  likely  to  be  of  cardiac  origin  than 
true  bronchial  asthma.  Expiration  is  not  likely  to  be  predominantly 
involved,  and  other  symptoms  of  cardiac  insufficiency  arc  usually 
present.  Careful  examination  of  the  heart  will  usually  determine  the 
diagnosis.  Renal  insufficiency  may  give  rise  to  a  type  of  dyspnea 
known  as  renal  or  uremic  asthma.  Here  too  the  respiratory  disturbance 
may  occur  suddenly.  Both  inspiration  and  expiration  are  affected. 
Other  symptoms  are  usually  present,  and  examination  of  the  heart, 
the  urine,  and  the  blood-pressure  will  establish  the  diagnosis. 

Prognosis. — An  asthmatic  paroxysm  of  itself  is  practically  never 
fatal.  Predictions  as  to  the  outcome  of  the  disease  are  very  uncertain. 
In  general  those  cases  are  most  favorable  in  which  a  determining  cause 
can  be  early  detected  and  removed.  The  patient's  willingness  or 
ability  to  seek  favorable  conditions  or  places  must  also  be  considered. 
Youth  is  of  favorable  moment.  A  disease  which  begins  in  childhood 
may  end  in  recovery  at  puberty.  Long  intervals  of  freedom  between 
attacks  of  diminishing  severity  are  hopeful.  On  the  other  hand  the 
onset  of  the  disease  after  forty  or  forty-five  years  is  seldom  followed 
by  full  recovery.  A  persistent  bronchial  catarrh  between  attacks  is 
likewise  unfavorable.  With  the  advent  of  such  complications  as 
chronic  bronchitis,  bronchiectasis,  emphysema,  cardiac  hypertrophy 
and  dilatation  the  prognosis  becomes  more  unfavorable. 

Treatment. — There  is  no  specific  treatment.  Further  study  of 
anaphylaxis  in  animals  may  lead  to  more  successful  therapy.  In  the 
majority  of  cases  the  disease  appears  to  run  its  course,  but  little  influ- 
enced by  the  numerous  measures  suggested  for  its  relief.  New  methods 
apparently  successful  in  isolated  or  small  groups  of  cases  have 
repeatedly  found  a  place  in  the  literature,  only  to  be  replaced  by  other 
and  still  newer  measures.  A  drug  which  appears  at  one  time  to  have 
afforded  relief  may  utterly  fail  at  the  next  trial  in  the  same  or  another 
patient.  The  more  distressing  features  of  the  paroxysms  can  often 
be  alleviated.  They  may  recur  at  longer  intervals  or  even  stop,  but 
it  is  difficult  to  estimate  the  influence  of  treatment  in  so  variable  a 
disease.  The  treatment  is  most  conveniently  considered  under  the 
following  headings: 

1.  The  Attack. — An  abundance  of  fresh  air  enables  the  patient  to 
breathe  more  easily.  An  upright  and  sitting  position,  with  the  elbows 
supported  on  the  arms  of  a  chair,  often  assists  him  in  his  efforts  to 
bring  the  accessory  muscles  of  respiration  into  play. 

Morphin  is  the  most  valuable  remedy  for  an  attack  of  asthma, 
but  the  possibility  of  inducing  its  habitual  use  must  always  be  borne 
in  mind.  Isolated  or  successive  attacks  of  great  severity  may  justify 
its  administration  by  the  physician  or  the  nurse  under  his  direction, 
but  it  should  never  be  left  in  the  hands  of  the  patient  to  prescribe 
for  himself.  The  subcutaneous  injection  of  morphin,  gr.  |  (0.010  gm.), 
gives  the  most  immediate  relief.    It  may,  if  necessary,  be  repeated  in 


BRONCHIAL  ASTHMA  61 

two  hours.  Larger  doses  may  be  required.  Atropin,  gr.  Ty0  (0.00054 
gm.),  may  well  be  combined  with  the  morphin.  Adrenalin  chloride, 
1  to  1000  solution,  0.5  to  1  c.c.  given  subcutaneously,  acts  well  in 
some  cases. 

Heroin,  gr.  ^V  (0.00325  gm.),  is  sometimes  an  efficient  substitute 
for  morphin.  Chloral  hydrate,  gr.  10  (0.650  gm.),  repeated  if  neces- 
sary in  an  hour,  may  be  successful,  but  should  not  be  used  in  patients 
with  weak  heart  because  of  its  depressing  effect  on  the  circulation. 
Bromides  may  also  be  used.  A  spray  of  cocain  hydrochlorate  (5  per 
cent.)  into  the  nasal  passages  and  throat  has  been  recommended. 
The  cocain  may  also  be  applied  by  means  of  a  cotton  swab  moistened 
in  the  solution,  or  a  few  drops  allowed  to  fall  into  each  nasal  cavity 
from  a  medicine  dropper.  As  with  morphin,  there  is  danger  of  inducing 
its  habitual  use,  and  its  administration  should  only  be  considered 
in  severe  cases,  and  then  only  at  infrequent  intervals.  Pilocarpin, 
gr.  |  (0.008  gm.),  has  been  found  to  be  efficient  at  times. 

In  mild  or  recurring  attacks,  inhalations  may  be  tried.  Many 
asthma  powders,  cigarettes,  and  medicated  papers  are  on  the  market. 
They  usually  contain  the  leaves  of  some  plant  belonging  to  the  family 
Solanacese,  to  which  potassium  nitrate  is  added  to  increase  their 
combustion.  Stramonium  and  belladonna  leaves  are  most  commonly 
used.  A  small  amount  of  powdered  stramonium  leaves  and  potassium 
nitrate,  of  each  equal  parts,  may  be  placed  on  a  metal  plate,  ignited, 
and  the  fumes  inhaled.  Graves'  often  quoted  experience  illustrates  the 
varying  susceptibility  of  patients.  Of  two  asthmatics  visited  on  one 
day  the  first  ascribed  his  attack,  the  second  his  relief,  to  a  smoking 
chimney.  It  is  unwise  to  prescribe  preparations  the  composition  of 
which  is  unknown.  Opium  or  Indian  hemp  enters  into  the  composi- 
tion of  some  of  them.  The  composition  of  some  of  the  more  popular 
mixtures  is  said  to  be  as  follows : 

"Poudre  Clery"  contains  powdered  opium  (3.0),  powdered  bella- 
donna, and  stramonium  leaves  (aa  45.0),  saturated  with  a  solution  of 
potassium  nitrate  (7.0)  and  distilled  water  (20.0). 

Fischer's  Antiasthmatic  Powder  consists  of  stramonium  leaves 
(250.0),  sweet  clover  flowers  (25.0),  potassium  nitrate  (50.0),  and  dis- 
tilled water  (250.0). 

Schiffmann's  Asthma  Powder  is  made  up  of  potassium  nitrate, 
stramonium  leaves,  and  the  root  of  skunk  cabbage. 

Reichenhaller  Powder  contains  stramonium,  potassium  nitrate, 
benzoin,  the  leaves  of  Grindelia  robusta,  and  eucalyptus. 

Espic's  Cigarettes  contain  belladonna  leaves  (60.0),  hyoscyamus, 
and  stramonium  leaves  (aa  30.0),  phellandrium  seeds  (10.0),  extract 
of  opium  (3.0),  and  cherry-laurel  water  a  sufficient  amount  (about 
two  volumes).  The  leaves  and  seeds  are  macerated  for  twelve  hours 
and  expressed,  the  extract  of  opium  then  dissolved,  bibulous  paper 
next  moistened  with  the  liquid  and  well  dried,  in  order  that  cigarettes 
may  be  made.  A  small  amount  of  nitre  is  added  to  the  infusion  to 
makes  the  cigarettes  burn  freely. 


62  DISEASES  OF   THE  BRONCHI 

"  ( 'arton  Fumigatoire,"  of  the  French  Codex,  contains  nitre  combined 
with  powdered  belladonna,  stramonium,  digitalis,  and  lobelia  leaves 
with  myrrh  and  oliban.    Pieces  of  the  paper  are  ignited  in  the  room. 

"Himrod's  Cure  for  Asthma"  is  said  to  be  well  imitated  as  follows: 
Powdered  lobelia,  black  tea,  and  stramonium  leaves,  of  each  one  ounce, 
to  which  two  ounces  of  a  saturated  solution  of  nitrate  of  potash  is 
added,  mixed,  and  dried. 

Trousseau,  himself  an  asthmatic,  and  unaccustomed  to  the  use  of 
tobacco,  often  found  a  few  puffs  of  an  ordinary  cigar  an  efficient  remedy. 
He  gives  the  following  prescription:  Belladonna  leaves  (0.36),  hyo- 
scyamus  (0.18),  phellandrium  aquaticum  (0.06),  and  stramonium 
(0.18).  The  leaves  are  carefully  stripped  from  the  ribs,  dried,  and 
treated  with  a  trace  of  extract  of  opium.  The  cigarette  papers,  pre- 
pared by  washing  in  cherry-laurel  water,  are  then  filled  with  the 
mixture. 

McPhedran1  cites  the  following  prescription:  Stramonium  leaves 
(8.0),  anise  (4.0),  tobacco  leaves  (0.2),  potassium  nitrate  (4.0),  a  tea- 
spoonful  of  which  is  ignited  in  an  open  vessel  and  the  fumes  inhaled. 

The  smoke  from  "Saltpetre  paper"  may  be  used.  This  is  prepared 
by  moistening  filter  paper  in  a  half-saturated  solution  of  potassium 
nitrate.  The  paper  is  dried  and  the  fumes  inhaled  after  ignition.  It 
may  also  be  rolled  into  cigarettes. 

Other  inhalations  are  used  as  follows:  The  smoke  from  cigarettes 
of  stramonium  and  camphor,  inhalation  of  amyl  nitrite  (3  to  5  minims 
in  capsules),  or  amyl  valerianate,  ether,  chloroform,  turpentine,  the 
fumes  of  ammonia,  the  vapor  of  warm  water,  to  which  compound 
tincture  of  benzoin  (1  dram  to  the  pint)  is  added,  oxygen,  pyridin 
(1  dram)  in  a  saucer  in  the  room,  or  5  to  10  drops  on  a  handkerchief 
about  the  neck. 

2.  Prevention  of  Recurrences. — This  is  difficult  and  at  times  impossible 
The  various  measures  may  be  considered  under  the  following  headings: 

(a)  Removal  of  the  Cause. — The  possibility  of  nasal  disease  as  a 
cause  of  asthma  must  always  be  considered,  and  pathologic  condi- 
tions here,  as  elsewdiere,  should  receive  appropriate  treatment.  The 
influence  of  reflex  irritation  from  more  remote  parts  of  the  body 
cannot  be  denied.  A  careful  inquiry  concerning  possible  exciting 
causes,  mentioned  under  Etiology,  may  suggest  certain  precautions 
against  recurrent  attacks. 

(b)  General  Treatment. — In  poorly  nourished  and  specially  in  neuras- 
thenic patients  an  improvement  of  the  general  nutrition  by  means 
of  abundant  food  and  fresh  air  is  most  helpful.  No  special  diet  can 
be  recommended.  Experience  teaches  many  patients  that  it  is  better 
to  avoid  a  hearty  evening  meal  and  to  wait  until  digestion  is  complete 
before  retiring.  In  some  patients  there  seems  to  be  a  relation  between 
flatulency  and  the  attacks,  and  those  foods  which  are  likely  to  lead 

1  Osier's  Modern  Medicine,  vol.  iii.         » 


BRONCHIAL  ASTHMA  63 

to  this  condition,  such  as  the  carbohydrates  and  fats,  may  well  be, 
limited.  Autosuggestion  is  capable  of  aggravating  and  in  some 
instances,  even  of  inducing  the  attacks  in  susceptible  individuals. 
In  such  cases  the  explanation  of  the  influence  of  a  fixed  impression 
and  the  substitution  of  a  hopeful  attitude  may  be  successful. 

(c)  Drugs. — The  iodid  of  potash  in  doses  of  gr.  5  to  15  (0.325  to 
0.975  gm.),  two  or  three  times  a  day,  beginning  at  once  after  the 
cessation  of  the  attack,  may  be  successful  in  delaying,  in  diminishing 
the  severity,  or  even  in  the  prevention  of  recurrences.  Arsenic  in  the 
form  of  Fowler's  solution  may  also  be  used.  A  course  of  atropin 
may  also  be  tried,  beginning  with  gr.  yts  (0.00054  gm.)  and  doubling 
the  dose  every  three  to  four  days  until  gr.  -^  (0.00216  gm.)  or  more  is 
reached  or  until  a  disturbance  of  accommodation  or  dryness  of  the 
throat  follows.  Strychnin  may  also  be  given  alone  or  combined  with 
the  atropin. 

(d)  Danger  of  Anaphylactic  Shock  following  the  Use  of  Diphtheria 
Antitoxin  in  Patients  with  Asthma. — Partial  or  complete  relief  from 
asthma  has  been  noted  to  follow  the  injection  of  diphtheria  anti- 
toxin in  a  considerable  number  of  instances.  Some  of  the  patients 
thus  relieved  have  been  subject  to  asthmatic  attacks  in  the  presence 
of  the  emanation  from  horses.  Many  unfortunate  experiences  have 
shown,  however,  that  the  administration  of  diphtheria  antitoxin  in 
patients  with  asthma,  and  especially  horse  asthma,  is  dangerous. 
Gillette1  collected  28  cases,  of  which  12  were  followed  by  collapse 
and  15  by  death  after  the  administration  of  horse  serum.  Of  the  28 
cases,  in  17  there  was  a  history  of  asthma,  and  in  one  each  a  previous 
history  of  cardiac  dyspnea,  of  sneezing  and  irritation  of  the  eyes  when 
about  a  horse,  of  hay  fever,  and  of  chronic  bronchitis.  Of  these  21 
cases,  10  were  followed  by  collapse,  10  by  death,  and  in  1  the  result 
is  not  stated.  Four  instances  of  death  and  one  of  collapse  following 
the  injection  of  diphtheria  antitoxin  in  patients  with  asthma  have 
been  brought  to  my  attention.  The  symptoms  closely  resemble  the 
anaphylactic  shock  produced  in  sensitized  animals  by  a  reinjection 
of  the  same  foreign  serum.  Immediately  following  the  injection  there 
may  be  irritation  of  the  skin  and  an  urticarial  rash,  sudden  and  intense 
dyspnea,  cyanosis,  sense  of  suffocation,  unconsciousness,  and  death 
within  a  period  of  less  than  ten  minutes,  Death  is  probably  due  to 
spasm  of  the  bronchioles,  as  in  anaphylaxis  in  animals.  All  patients 
for  whom  the  use  of  diphtheria  antitoxin  is  under  consideration  should 
be  questioned  regarding  a  previous  history  of  asthma  or  susceptibility 
to  the  presence  of  horses.  Prophylactic  injection  of  serum  should,  if 
possible,  be  avoided  when  there  is  ground  for  suspecting  anaphylaxis. 
In  such  cases,  when  it  is  deemed  necessary  to  give  antitoxin  for  prophy- 
laxis or  treatment  against  diphtheria,  the  patient's  susceptibility  may 
be  tested  by  the  application  of  diphtheria  antitoxin  to  the  skin,  as  in 

1  Therapeutic  Gazette,  1909,  S.  3,  xxv,  159. 


64  DISEASES  OF  THE  BRONCHI 

von  Pirquet's  cutaneous  test  with  tuberculin  or  by  the  subcutaneous 

injection  of  a  small  dose  (0.1  c.c.)  of  the  serum.  Hypersusceptibility 
may  be  demonstrated  by  the  appearance  of  a  reaction  within  a  half- 
hour  of  the  use  of  the  serum.  It  may  be  that  in  sensitive  individuals, 
anaphylaxis  can  be  prevented  by  the  injection  of  a  small  dose  and  the 
use  of  the  serum  for  therapeutic  purposes  in  the  refractory  stage  which 
follows.  Besredka  and  Lissofsky1  found  that  guinea-pigs  sensitized 
to  serum  could  be  rendered  immune  to  an  otherwise  fatal  dose  by 
previous  injection  of  a  minute  quantity.  In  their  experiments,  four 
hours  were  required  to  produce  the  refractory  stage  by  subcutaneous 
injection.  Atropin  in  full  doses  may  be  successful  in  preventing  or 
relieving  anaphylaxis. 

(e)  Immunization  of  Patients  Susceptible  to  Egg  Albumen. — Schloss2 
noted  that  the  symptoms  of  egg  poisoning  in  his  patient  were  those 
of  anaphylaxis.  In  a  child  who  was  poisoned  whenever  he  ate  eggs, 
oatmeal,  or  almonds  an  urticarial  wheal  could  be  produced  by  the 
application  to  the  skin  of  the  protein  of  any  one  of  these  substances. 
Immunization  to  egg  white  was  secured  by  the  administration  by 
mouth  of  gradually  increasing  doses  of  ovomucoid  in  capsules.  Im- 
munization to  oatmeal  and  diminished  susceptibility  to  almonds 
were  coincident.  Talbot3  detects  hypersensitiveness  to  eggs  in 
children  by  the  appearance  of  an  urticarial  wheal  after  rubbing  white 
of  egg  into  the  unbroken  or  scarified  skin,  previously  cleaned  with 
soap  and  water  and  with  alcohol.  Egg  may  be  removed  from  the 
diet  or  insensitiveness  secured  by  the  administration  of  gradually 
increasing  doses  of  egg  albumen  in  capsules. 

(/)  Climate. — An  assurance  of  relief  cannot  be  promised  in  any 
climate,  and  yet  a  change  of  location  is  sometimes  successful  in  pre- 
venting recurrences.  City  is  often  better  than  country  life.  A  change 
from  one  place  to  another  nearby  may  be  as  beneficial  as  to  a  resort  far 
away.  Patients  whose  financial  condition  will  permit,  may  well  try 
one  location  after  another.  In  general  a  mild  and  equable  climate 
is  to  be  preferred,  and  thus  Florida,  Southern  California,  the  Riviera, 
and  Egypt  may  be  favorable.  Poorly  nourished  and  neurasthenic 
patients  may  be  benefited  by  a  stay  in  a  well-regulated  sanitarium. 
In  such  institutions,  psychotherapy,  pneumotherapy,  electrotherapy, 
and  hydrotherapy  may  be  added  to  the  prescriptions. 

1  Ann.  de  l'lnst.  Past.,  vol.  xxiv,  No.  12. 

2  Am.  Jour.  Dis.  of  Children,  1912,  p.  341. 

3  Bost.  Med.  and  Surg.  Jour.,  November  5,  1914. 


CHAPTER   III. 
BRONCHITIS  FIBRINOSA. 

This  has  also  been  termed  plastic  bronchitis,  bronchitis  pseudo- 
membranosa,  and  bronchial  croup.  It  is  characterized  by  the  forma- 
tion of  casts  within  the  bronchi. 

Occurrence. — The  cases  are  rare.  The  literature  was  collected  to 
1869  by  Lebert,1  who  found  44  cases.  West2  added  54  more  to  1889, 
and  in  1902  Bettmann3  brought  the  number  reported  since  Lebert's 
review  to  145.  Posselt4  gives  a  summary  of  the  literature  and  a  short 
account  of  the  reported  cases  since  1900. 

Classification. — A  division  of  the  cases  into  two  groups  according 
to  the  predominance  of  fibrin  or  mucus  in  the  casts  has  been  made  by 
Posselt,5  and  at  times  maintained  in  later  descriptions.  Frankel6 
separates  from  the  cases  of  essential  fibrinous  bronchitis  those  in  which 
there  is  the  formation  of  mucous  casts,  and  suggests  the  term  bronchitis 
pseudomembranacea  mucinosa  to  indicate  such  cases.  These  he  believes 
should  be  included  among  cases  grouped  as  bronchial  asthma.  A 
sharp  distinction  between  these  two  groups  cannot  be  maintained  on 
the  basis  of  the  composition  of  the  casts,  which  probably  always 
contain  both  fibrin  and  mucus  in  somewhat  varying  proportion. 
Moreover,  the  fibrinous  form  of  bronchitis  may  develop  in  the  course 
of  bronchial  asthma. 

A  grouping  of  the  cases  may  also  be  made  into  those  which  are 
secondary  to  some  recognizable  disturbance  of  the  lungs  or  other  organs 
and  those  which  are  primary  or  without  discoverable  association  with 
other  conditions. 

A  distinction  is  often  made  between  acute  and  chronic  forms  of  the 
disease.  In  the  former  there  is  only  one  attack,  while  in  the  latter 
there  are  recurrences  at  longer  or  shorter  intervals. 

Etiology. — The  condition  may  occur  at  any  age,  but  appears  to  be 
less  often  observed  in  the  old.  Males  are  more  frequently  affected 
than  females.  Cases  are  more  often  observed  in  the  colder  months 
of  the  year. 

Cases  occurring  in  the  course  of  acute  or  chronic  bronchopulmonary 
infection  form  the  largest  single  group.  In  a  considerable  number 
of  the  instances  in  this  class  the  clinical  manifestations  are  those  of 

1  Ueber  das  Vorkommen  fibrinoser  Entziindungsproduckte  in  den  Bronchien  und 
Lungenalveolen,  Deut.  Arch.  f.  klin.  Med.,  Bd.  vi,  p.  74. 

2  Practitioner,  1889,  xliii,  83.  3  Amer.  Jour.  Med.  Sci.,  1902,  cxxiii,  304. 
4  Med.  Klinik,  1909,  Nos.  33  and  34.          *  Prager  med.  Woch.,  1899. 

6  Spez.  Path.  u.  Ther.  d.  Lungenkrankheiten,  1904. 
5 


till  DISEASES  OF   THE  BRONCHI 

simple  chronic  or  acute  bronchitis.  Pulmonary  tuberculosis  occupies 
a  prominent  place  among  the  infections.  Lehmann-Model1  found 
tuberculosis  associated  in  10  of  20  autopsies  reported  on  cases  with 
fibrinous  bronchitis.  Of  his  6  cases,  3  showed  tuberculosis  at  autopsy. 
Extension  of  the  fibrinous  exudate  from  the  lung  to  the  smaller  and 
even  the  larger  bronchi  is  occasionally  observed  in  lobar  pneumonia 
with  the  expectoration  of  delicate  fibrinous  casts  of  the  bronchi. 
The  condition  is  at  times  observed  as  a  complication  of  typhoid 
fever,  measles,  and  scarlet  fever;  in  rare  instances  with  erysipelas, 
variola,  articular  rheumatism,  and  influenza.  Diphtheria  is  an  impor- 
tant cause,  the  fibrinous  bronchitis  being  most  often  part  of  a  descend- 
ing infection,  the  primary  manifestations  of  which  are  in  the  pharynx 
and  larynx.  Primary  involvement  of  the  deeper  parts  of  the  tract 
are  observed  in  rare  instances.  Of  220  autopsies  on  cases  with  diph- 
theria, Councilman,  Mallory,  and  Pearce2  found  membranous  deposits 
in  the  bronchi  in  43.  Rupture  of  caseous  lymph  glands  into  the  bronchi 
was  a  cause  in  Weigert's3  2  cases.  Actinomycosis  of  the  lung  compli- 
cated by  fibrinous  bronchitis  is  reported  by  Finckh.4  In  the  case 
reported  by  Devillers  and  Renon,5  greenish  membranes  composed  of 
the  mycelium  of  Aspergillus  fumigatus  were  expectorated.  The  patient 
selected  seeds  for  cultivation  by  testing  them  with  her  teeth. 

Fibrinous  bronchitis  is  reported  in  rare  instances  following  the 
inhalation  of  steam,  the  fumes  of  ammonia,  and  smoke.  Vintras8 
reported  the  occurrence  of  casts  as  a  complication  of  an  epithelioma 
of  the  esophagus  with  compression  of  the  trachea  in  the  region  of  the 
bifurcation.  In  Cesaris-Demel's7  case  there  was  an  aneurysm  of  the 
aorta,  with  compression  of  the  root  of  the  lung.  Fibrinous  casts  were 
found  at  autopsy  in  the  atelectatic  lung. 

A  relation  between  bronchitis  fibrinosa  and  bronchial  asthma  has 
been  noted.  In  a  small  proportion  of  the  cases  bronchitis  fibrinosa 
develops  in  the  course  of  bronchial  asthma,  and  with  Charcot-Leyden 
crystals,  Curschmann's  spirals,  and  eosinophils  in  the  sputum. 
Small  fibrinous  structures  are  not  infrequently  found  in  the  sputum 
in  asthma.  In  LiebermeisterV  and  in  Bettmann's9  cases  the  casts 
terminated  in  Curschmann  spirals.  In  Vierordt's10  case,  Curschmann's 
spirals  were  demonstrated  in  thesputum  after  the  casts  had  disappeared. 

Organic  disease  of  the  heart  with  failure  of  compensation  is  compli- 
cated by  fibrinous  bronchitis  in  a  small  number  of  cases.  Passive 
congestion  of  the  bronchi  and  lung  may  be  regarded  as  a  predisposing 

1  Ueber  Bronchitis  fibrinosa,  Inaug.  Diss.,  Freiburg,  1890. 

2  A  Study  of  the  Bacteriology  and  Pathology  of  Two  Hundred  and  Twenty  Fatal 
Cases  of  Diphtheria,  Boston,  1901,  p.  93. 

3  Virchow's  Arch.,  Bd.  lxxvii,  p.  294. 

4  Beitr.  z.  Chir.,  1904,  Bd.  xli,  Heft  3,  p.  676.  6  La  presse  med.,  1899. 

6  Lancet,  September  15,  1900,  p.  809. 

7  Giorn.  della  R.  Accad.  di  med.  di  Torino,  1900,  p.  577. 

8  Munch,  med.  Woch.,  1904,  xvii,  781.  9  Loc.  cit.,  p.  324. 
"J  Berl.  klin.  Woch.,  1883,  No.  29. 


BRONCHI  TIS  FI  BRINGS  A 


07 


factor  in  this  group.  The  evacuation  of  a  large  pleural  exudate  may 
be  followed  by  pulmonary  edema  and  the  expectoration  of  casts.  Jn 
rare  instances  the  condition  has  been  observed  in  association  with 
diseases  of  the  skin,  such  as  impetigo  capitis,  herpes  zoster,  herpes  of 
the  lips,  throat  and  pharynx  and  pemphigus.  In  Mader's1  case  there 
was  pemphigus  of  the  mucous  membrane  of  the  mouth,  throat,  and 
conjunctiva.  Extension  to  the  larynx  was  accompanied  by  dyspnea 
and  the  expectoration  of  bronchial  casts.  Death  followed  two  years 
after  the  onset  of  the  respiratory  disturbances.  An  apparent  relation 
with  menstruation  has  been  noted  in  rare  instances. 


Fig.  11 


Expectorated  cast  from  a  case  of  fibrinous  bronchitis.     Three-fourths  natural  size. 
Drawn  from  fresh  specimen.      (After  Bettrnann.) 

Cases  unassociated  with  any  apparent  disturbance  of  the  bronchi, 
lungs,  or  other  organs,  to  which  the  fibrinous  bronchitis  can  be  regarded 
as  secondary,  form  a  small  group.  Such  cases  are  classed  as  primary 
or  idiopathic  fibrinous  bronchitis. 


1  Wiener  med.  Woch.,  1882,  Nos.  11  to  14. 


68  DISEASES  OF   THE  BRONCHI 

The  conditions  with  which  bronchitis  fibrinosa  are  associated  are 
variable  and  in  many  instances  can  be  regarded  as  little  more  than  a 
coincidence.  In  the  majority  of  the  cases,  however,  the  bronchial 
casts  develop  in  the  course  of  diseases  in  which  the  bronchial  mucosa 
may  be  assumed  already  to  have  suffered  some  injury  of  an  inflamma- 
tory, mechanical,  or  toxic  character,  and  it  is  natural  to  suspect  that 
herein  may  lie  the  predisposing  cause  of  the  disease.  Basing  his  con- 
tention on  Weigert's1  observation  that  destruction  of  the  protective 
epithelium  is  a  fundamental  condition  for  the  development  of  a  fibrin- 
ous pseudomembrane  on  the  surface  of  mucous  membranes,  Frankel2 
asserts  that  fibrinous  exudation  into  the  bronchial  lumen  can  occur 
only  when  the  epithelium  is  destroyed  or  sufficiently  altered  to  allow 
the  passage  of  fibrin-forming  material.  Small  defects  may  permit  the 
outflow  of  coagulable  material  and  its  diffusion  over  still  intact  parts 
of  the  tract.  To  this  Midler3  raises  the  objection  that  evidence  of  loss 
of  bronchial  epithelium  is  lacking.  The  fact  that  the  disease  may 
last  for  years  without  any  substantial  injury  does  not  suggest  a  deep 
alteration  of  the  bronchial  surface,  and  severe  bronchitis  and  broncho- 
pneumonia with  destruction  of  the  bronchial  epithelium  often  occur 
without  the  formation  of  fibrin.  Josue  and  Paillard4  obtained  coagu- 
lation in  a  solution  of  mucin  by  the  addition  of  a  glycerin  extract  of 
the  patient's  expectoration  and  the  casts.  Glycerin  extracts  of  the 
expectoration  of  other  subjects  proved  relatively  less  active.  Observa- 
tions on  the  phenomena  of  coagulation  by  Bordet  and  Delange5 
may  throw  light  on  the  formation  of  bronchial  casts. 

Evidence  in  favor  of  any  constant  or  necessary  bacterial  infection 
is  lacking.  Attempts  to  produce  the  disease  experimentally  in  animals 
by  the  introduction  of  bacteria  into  the  trachea  have  proved  negative. 

Pathology. — A  considerable  number  of  autopsies  have  been  per- 
formed on  patients  with  fibrinous  bronchitis,  but  few  investigators 
have  interested  themselves  in  other  than  the  gross  changes.  More 
complete  studies  are  desirable  and  an  investigation  of  the  condition 
of  the  mucous  membrane  of  the  tract.  If  casts  have  been  expectorated, 
none  may  be  found  at  autopsy.  Intact  casts  or  their  fragments  may 
be  found,  lying  free  in  the  bronchial  lumen  or  in  places  adherent  to 
the  wall.  The  bronchial  involvement  may  be  diffuse  and  include  all 
branches  even  to  their  finest  ramifications  or  involve  only  a  circum- 
scribed region.  Diffuse  involvement  and  failure  to  expectorate  the 
casts  with  fatal  asphyxia  as  a  result  is  more  common  in  the  acute 
cases. 

Changes  in  the  bronchial  wall  may  apparently  be  limited  to  swelling 
and  redness  of  the  mucosa.    Rollet6  found  tubercles  in  the  wall  of  the 


1  Ueber  Krupp  und  Diphtheritis,  Virchow's  Arch.,  Bd.  lxxii,  p.  253. 

2  Loc.  cit.,  p.  117.  3  Deut.  Klinik,  1903-07,  p.  261. 
«  Bull,  et  mem.  Soc.  Med.  d.  Hop.  de  Paris,  1909,  3  s.,  xxviii,  97. 

6  Ann.  d.  l'Inst.  Pasteur,  1912,  Nos.  9  and  10. 
6  Wien.  med.  Woch.,  1866,  Nos.  20  and  21. 


BRONCHITIS  FIBRIN  OS  A  69 

bronchus.  Lehmann-Moclel1  found  caseous  infiltration  of  the  wall  of 
the  bronchus  containing  a  cast.  Kretschy2  found  loss  of  epithelium 
and  infiltration  with  white  cells  in  the  region  of  a  cast  in  situ.  Iloch- 
haus3  demonstrated  small  defects  in  the  mucous  membrane  of  the 
larger  bronchioles  and  infiltration  of  the  wall  with  leukocytes. 
Grandy's4  observations  are  of  special  interest.  The  cast  was  found  in 
situ.  The  mucous  glands  were  dilated  with  mucus  which  could  be 
seen  to  extend  from  the  excretory  ducts  and  merge  with  the  bronchial 
casts.  Leukocytic  infiltration  was  noted  about  the  bases  of  the  mucous 
glands  and  in  the  peribronchial  tissue.  Goblet  cells  were  present  in 
large  numbers.  Schlittenheim5  made  a  careful  study  of  a  case  with 
pulmonary  tuberculosis.  Fibrin  and  desquamated  epithelial  cells 
were  found  in  the  alveoli  and  the  bronchi  of  the  right  lower  lobe. 
The  mucous  glands  were  dilated  and  contained  desquamated  cells 
and  mucus,  and  the  peribronchial  tissue  was  infiltrated  with  leukocytes. 

Symptoms. — Dyspnea,  cough,  and  the  expectoration  of  casts  are 
the  principal  symptoms.  Symptoms  of  bronchial  catarrh  usually 
precede  and  follow  the  attack.  One  or  more  chills  may  initiate  the 
paroxysm.  In  a  small  proportion  of  the  cases  there  are  no  preliminary 
symptoms.  The  dyspnea  and  cough  are  commonly  paroxysmal  and 
last  for  from  twenty-four  to  forty-eight  hours  before  the  casts  are 
expectorated.  The  cough  is  severe  and  dry  unless  the  condition  com- 
plicates bronchopulmonary  disease  associated  with  expectoration. 
Hoarseness  is  absent  unless  the  larynx  is  involved.  The  dyspnea 
is  due  to  the  accompanying  catarrh,  passive  hyperemia  of  the  lung, 
or  bronchial  obstruction.  Suffocation  rarely  occurs  owing  to  the  limi- 
tation of  the  process  to  certain  bronchi  only,  but  in  Fagge's6  case 
death  occurred  from  occlusion  of  the  bronchi  at  the  bifurcation  of  the 
trachea.  In  some  instances  cough  and  dyspnea  are  absent.  Expulsion 
may  be  affected  by  hawking.  A  feeling  of  tightness  or  oppression  is 
often  experienced.  Pain  is  usually  absent.  When  present  it  may  be 
due  to  the  violence  of  the  cough,  and  in  rare  instances  is  referred  to 
the  apparent  seat  of  formation  of  the  casts.  The  expectoration  of  casts 
usually  lasts  for  several  days,  after  which  there  is  relief  of  the  symp- 
toms. Moderate  elevation  of  temperature  is  often  observed,  and  may 
be  seen  not  only  in  the  secondary,  but  also  in  the  primary  cases. 

Certain  differences  between  the  acute  and  chronic  cases  may  be 
noted.  The  acute  cases  are  less  frequent  and  usually  more  severe  with 
fever,  paroxysmal  cough,  marked  dyspnea,  oppression  and  feeling 
of  suffocation.  Cyanosis  may  be  intense.  The  severity  of  the  symp- 
toms in  this  form  is  due  to  the  formation  of  casts  over  a  wider  extent 
of  bronchial  territory.    In  severe  cases  with  widespread  involvement, 

1  Loc.  cit.  2  Wien.  med.  Woch.,  1873,  Nos.  14,  15,  and  16. 

3  Deut.  Arch.  f.  klin.  Med.,  Bd.  lxxiv,  p.  11. 

4  Centralbl.  f.  allg.  Path.  u.  path.  Anat.,  vol.  viii,  p.  513. 
6  Deut.  Arch.  f.  klin.  Med.,  1900,  Bd.  lxvii. 

6  Trans.  Path.  Soc.  London,  vol.  xvi,  p.  48. 


70  DISEASES  OF  THE  BRONCHI 

efforts  to  expel  the  easts  may  be  ineffectual.  Increasing  dyspnea, 
cyanosis,  and  somnolence  may  then  terminate  in  death  from  asphyxia. 
The  duration  of  the  primary  acute  cases  is  usually  from  one  to  three 
weeks. 

The  chronic  eases  are  more  frequent  and  less  severe.  The  onset  is 
more  gradual  and  may  be  long  preceded  by  symptoms  of  chronic 
bronchitis  interrupted  at  varying  intervals  by  attacks  of  paroxysmal 
cough,  dyspnea,  and  oppression,  followed  by  the  expectoration  of 
casts  and  relief.  Fever  is  usually  absent.  In  this  form  the  process  is 
more  often  circumscribed,  and  the  casts  may  be  so  small  and  easily 
detached  as  to  give  rise  to  no  dyspnea.  The  number  and  duration 
of  the  attacks  is  very  variable.  They  may  recur  daily  or  at  intervals 
of  days,  weeks,  months  or  years. 

On  physical  examination  there  may  be  no  other  signs  than  those 
of  bronchial  catarrh  which  may  be  diffuse  or  limited  to  the  involved 
region.  In  outspoken  and  typical  cases,  the  signs  are  those  of  broncho- 
stenosis. On  inspection  there  may  then  be  diminished  excursion  of  the 
affected  side.  Percussion  is  usually  negative,  but  dulness  may  be 
present  from  atelectasis  or  pulmonary  infiltration.  On  auscultation, 
diminished  or  absent  respiratory  murmur  may  be  noted  over  the  region 
supplied  by  the  occluded  bronchus  with  return  of  the  breath  sounds 
alter  expulsion  of  the  casts.  Sonorous  or  sibilant  rales  may  be  limited 
to  the  affected  region.  In  rare  instances  peculiar  flapping  sounds  due 
to  the  partial  detachment  of  the  casts  may  be  heard.  The  lower  lobes 
are  most  often  affected.  The  signs  of  emphysema  may  be  present  in 
uninvolved  parts  of  the  lung.  In  Mader's1  case  laryngoscopic  examina- 
tion disclosed  the  presence  of  a  membrane  in  the  pharynx  and  on  the 
epiglottis.  In  West's2  case  the  percussion  note  was  greatly  impaired 
over  the  whole  left  side;  the  voice  and  respiration  were  everywhere 
absent  with  the  exception  of  the  left  interscapular  region,  where  they 
were  somewhat  exaggerated.  The  heart  was  displaced  toward  the 
affected  side.  After  the  expulsion  of  the  cast  the  upper  part  of  the  left 
lung  became  resonant,  and  the  breath  sounds  distinct,  while  the  base 
remained  dull.    The  apex  of  the  heart  returned  to  the  nipple  line. 

The  sputum  is  variable  in  amount  and  character,  but  is  usually 
scanty  and  mucopurulent,  at  times  blood-streaked  or  frankly  hemor- 
rhagic. Hemoptysis  may  precede  or  accompany  the  expectoration 
of  casts.  Small  amounts  of  blood  may  come  from  the  rupture  of  the 
attachments  of  the  cast  to  the  bronchial  wall.  Large  amounts  prob- 
ably come  from  the  lung. 

The  casts  are  usually  found  as  nondescript  masses  which,  if  small, 
may  be  readily  overlooked,  and  must  first  be  carefully  unrolled  in 
water  before  their  identity  can  be  established.  The}-  vary  in  thickness 
from  a  few  millimeters  to  a  centimeter  and  a  half  and  in  length  up  to 
six  or  seven  inches.    From  one  to  a  dozen  or  more  may  be  expectorated 

i  Wiener  med.  Woch.,  1882,  Nos.  11  to  14.  2  Lancet,  1908,  i,  489. 


BRONCHITIS  FI  BRINGS  A  71 

daily.  They  are  usually  pearl  gray  or  white,  at  times  of  a  reddish 
color.  The  larger  casts  are  firm,  the  smaller  soft  in  consistency.  They 
are  for  the  most  part  of  cylindrial  form,  at  times  flattened,  and  are 
branched  in  accordance  with  the  divisions  of  the  bronchi  in  which 
they  arise.  A  rapid  division  into  short  branches  suggests  an  origin 
from  the  upper  parts  of  the  bronchial  tree,  while  a  more  gradual 
division  and  longer  branches  suggests  an  origin  from  the  lower  parts 
of  the  lung,  as  noted  by  Biermer.1  The  finest  divisions  may  be  pointed, 
cork-screw-like,  and  resembling  Curschmann's  spirals,  or  show  small 
clubbed  terminations  representing  molds  of  the  infundibula.  Their 
surface  is  usually  smooth,  but  the  inclusion  of  air-bubbles  may  lead 
to  the  production  of  nodular  swellings  and  a  beaded  appearance. 
The  thicker  branches  and  the  smallest  ramifications  are  usually  solid, 
while  those  of  intermediate  size  are  not  infrequently  hollow  and  filled 
with  air  and  mucus.  On  section  of  the  larger  branches  of  the  casts, 
a  concentric  and  folded  lamination  may  be  observed,  and  represents 
the  deposition  of  the  material  of  which  it  is  composed  in  layers,  the 
innermost  ring  being  the  oldest. 

Microscopic  examination  of  casts  shows  a  varying  number  of  fine 
fibrillar  and  an  interlacing  network  of  fibers  in  a  ground  substance 
composed  of  a  structureless,  hyaline  material  containing  mononuclear 
and  polynuclear  leukocytes,  fat  droplets,  occasional  eosinophiles, 
and  alveolar  epithelium  and  isolated  ciliated  cylinder  cells.  Red- 
blood  cells  are  rarely  found  within  the  substance  of  the  cast,  but  are 
not  infrequent  on  its  surface.  Mast  cells  are  found  in  rare  instances. 
Charcot-Leyden  crystals  and  Curschmann  spirals  are  occasionally 
found  in  the  casts.  Bacteria  may  or  may  not  be  demonstrable.  The 
pneumococcus,  Friedlander's  bacillus,  streptococcus,  and  staphylo- 
coccus pyogenes  albus  and  aureus  have  been  found  in  primary 
cases,  and  the  pneumococcus,  diphtheria  bacillus,  tubercle  bacillus, 
and  influenza  bacillus  in  secondary  cases.  The  bacteriologic  findings 
are  so  inconstant  as  to  indicate  that  the  formation  of  the  casts 
cannot  be  ascribed  to  the  influence  of  any  one  organism. 

Various  chemical  tests  have  been  used  for  the  determination  of  the 
fibrinous  or  mucous  character  of  the  casts,  but  their  interpretation  is 
difficult.  Fibrin  swells  in  dilute  acetic  acid,  in  potassium  hydrate 
and  in  hydrochloric  acid,  and  is  digested  at  body  temperature  by 
artificial  gastric  juice  (pepsin-hydrochloric  acid),  while  mucus  is 
resistant  against  these  reagents.  Fibrin  may  be  stained  by  Weigert's 
method,  but  mucus  does  not  stain.  Thionin  is  used  as  a  stain  for  mucus 
by  Hoyer2  and  Hari.3  Brilliant  green  and  neutral  red  are  used  by 
Hecht.4     Miiller5  finds  that  the  pure  mucus  of  the  respiratory  tract 

1  Virchow's  Handb.  d.  spec.  Path.  u.  Ther.,  Bd.  v. 

2  Arch.  f.  mikr.  Anat.,  1890,  Bd.  xxxvi. 

3  Ibid.,  1901,  Bd.  lviii. 

4  Wiener  klin.  Woch.,  1908,  No.  45. 
6  Deut.  Klinik.,  1904,  p.  261. 


72  DISEASES  OF  THE  BRONCHI 

splits  into  36  per  cent,  glucosamin  while  bronchial  casts  contain  66 
per  cent,  mucin. 

Diagnosis.— This  can  be  made  with  certainty  only  by  the  expec- 
toration of  branching  casts  of  the  character  already  described.  Small 
casts  may  be  readily  overlooked  unless  the  sputum  is  carefully  inspected 
and  the  attempt  is  made  to  unroll  any  solid  particles  or  masses  after 
suspension  in  water.  Confusion  with  blood-clot  is  possible  unless  this 
is  done.  Microscopic  examination  will  assist  in  the  identification  of 
small  particles  without  branching.  In  the  absence  of  branching,  small 
laminated  particles  of  casts  may  be  mistaken  for  fragments  of  echino- 
coccus  cyst  membrane. 

When  casts  are  absent  from  the  sputum,  the  diagnosis  may  be  sus- 
pected in  patients  with  a  previous  history  of  fibrinous  bronchitis  and 
symptoms  of  bronchostenosis.  Without  a  history  of  previous  attacks, 
the  distinction  from  other  and  more  common  causes  of  broncho- 
stenosis is  difficult  or  impossible.  Bronchial  occlusion  by  tenacious 
secretion  in  children  with  capillary  bronchitis  and  bronchopneumonia 
is  more  transient  and  oftentimes  relieved  by  vigorous  cough.  A  careful 
history  and  physical  examination,  .r-ray  examination  and  the  Wasser- 
mann  test  will  assist  in  the  exclusion  of  foreign  body,  syphilis,  and 
aneurysm.  The  sputum  should  be  carefully  examined  for  tubercle 
bacilli,  actinomyces,  and  diphtheria  bacilli.  Laryngoscopic  and  bron- 
choscopic  examination  may  make  the  diagnosis  possible. 

Prognosis. — The  immediate  outlook  is  less  favorable  in  the  acute 
than  in  chronic  cases,  and  worse  in  children  than  in  adults.  Death 
occurs  in  about  half  of  the  acute  cases.  The  extent  of  the  bronchial 
involvement,  the  strength  of  the  patient  and  the  character  of  the  under- 
lying disease  in  secondary  cases  must  be  considered  in  estimating 
the  prognosis  of  individual  patients.  In  chronic  cases  the  prognosis 
for  life  is  relatively  favorable,  death  occurring  in  only  four  of  36  cases 
collected  by  Championniere!1  Recurrences  are  frequent  in  this  form. 
Even  long  intervals  of  freedom  cannot  be  regarded  as  an  assurance 
against  a  return  of  the  disease.  In  Brik's2  case  following  the  first 
attack  at  thirty-six,  the  disease  recurred  at  forty-one,  forty-two,  and 
sixty.  In  Kisch's3  remarkable  case,  attacks  recurred  at  intervals  for 
twenty-five  years. 

Treatment. — There  is  no  specific  treatment.  The  indications  are 
to  remove  or  assist  in  the  removal  of  the  casts  and  prevent  their 
subsequent  formation.  Neither  indication  can  be  satisfactorily  met. 
Provided  the  strength  of  the  patient  permits,  the  subcutaneous 
injection  of  apomorphin  hydrochlorate  may  be  used.  Iodid  of  potash 
internally  has  seemed  to  be  effective  in  some  cases.  Inhalations  of 
warm  steam  or  a  spray  of  lime  water  may  be  tried.  The  lime  water 
(25)  may  be  combined  with  solution  of  sodium  hydrate  (2)  and  water 

1  De  la  bronchite  pseudomembraneuse  chronique,  These  de  Paris,  1876. 

2  Wiener  med.  Presse,  1882,  p.  828. 

3  Prager  med.  Woch.,  1888,  xiii,  69. 


BRONCHITIS  FIBRIN  OS  A  73 

(200) .  Whether  a  dissolving  action  on  the  cast  in  situ  can  be  effected 
by  such  means  is  doubtful.  Compression  of  the  chest  by  the  hand 
during  expiration  has  also  been  recommended.  While  the  bronchial 
cast  is  still  unexpelled,  the  patient  is  in  danger  of  suffocation  from 
occlusion  of  the  bronchi  at  the  tracheal  bifurcation  or  impaction  of 
a  detached  cast  in  the  glottis.  The  possibility  of  removal  of  a  cast 
by  bronchoscopy  should  be  entertained  and  may  be  life  saving  in  these 
cases.  To  prevent  recurrence  attention  must  be  paid  to  the  removal 
of  the  cause  if  this  can  be  discovered.  The  prevention  and  treatment 
of  bronchial  catarrh  must  be  considered  in  this  connection. 


CHAPTER   IV. 
BRONCHITIS  OBLITERANS. 

In  1901,  Lange1  first  recognized  the  existence  anatomically  of  con- 
nective-tissue occlusion  of  the  finer  bronchi,  bronchitis  and  bronchio- 
litis obliterans,  as  a  relatively  independent  affection  and  unassociated 
with  extensive  involvement  of  the  lung.  Soon  after  his  publications, 
Frankel2  made  the  diagnosis  of  the  condition  during  life  in  a  patient 
suffering  from  severe  dyspnea  following  the  inhalation  of  the  fumes  of 
nitrous  acid. 

Etiology. — In  addition  to  Frankel's  first  case,  similar  changes 
have  been  observed  following  the  inhalation  of  the  fumes  of  nitrous 
acid  with  chlorine  by  Edens,3  plaster  of  Paris  by  Frankel,4  and  after 
phosphorus  poisoning  by  Schmorl.5  Similar  pathologic  changes 
were  observed  by  Hart6  following  measles  and  whooping  cough  in 
children.  In  Schmorl's7  case  with  tertiary  syphilis,  isolated  organisms 
morphologically  like  the  spirochaeta  of  syphilis  were  found  in  the  peri- 
bronchial granulation  tissue.  Colombino8  has  reported  the  condition 
after  diphtheria.  Pernice9  at  times  found  obliteration  of  the  bronchioles 
after  apparently  uncomplicated  catarrhal  bronchitis.  Miiller10  regards 
the  condition  as  a  development  in  the  course  of  especially  severe  forms 
of  acute  or  subacute  bronchiolitis,  and  refers  to  two  cases.  Circum- 
scribed obliterative  bronchiolitis  may  follow  lobar  pneumonia.  In 
Wegelin's11  case  of  a  boy  who  died  eight  weeks  after  the  aspiration 
of  a  plum-stone,  obliterating  bronchitis  and  bronchiolitis  were  found 
in  many  of  the  smallest  bronchi  and  bronchioli  of  the  right  lung. 

Pathology. — Of  special  importance  in  the  production  of  character- 
istic symptoms  is  the  diffusion  of  the  process  over  the  greater  part  of 
the  bronchioli  of  both  lungs,  in  contrast  to  the  more  circumscribed 
but  otherwise  apparently  similar  changes  which  at  times  follow  pneu- 
monia.    The  disturbance  is  predominantly  an  involvement  of  the 

1  Ueber  eine  eigenthiimliche  Erkrankung  der  kleinen  Bronehien  und  Bronchiolen 
(Bronchitis  et  Bronchiolitis  obliterans),  Deut.  Arch.  f.  klin.  Med.,  Bd.  lxx,  p.  342. 

2  Ueber  Bronchiolitis  fibrosa  obliterans  nebst  Bemerkungen  iibcr  Lungenhyperamie 
und  indurierende  Penumonie,  ibid.,  Bd.  lxxiii,  p.  484. 

3  Deut.  Arch.  f.  klin.  Med.,  1905-06,  lxxxv,  598. 

4  Verhandl.  d.  Berl.  med.  Gesellsch.,  1908,  xxxix,  460. 
6  Quoted  from  Colombino,  Deut.  med.  Woch.,  1910. 

6  Deut.  Arch.  f.  klin.  Med.,  1903-04,  lxxix,  108. 

7  Verhandl.  d.  deut.  path.  Gesellschaft,  1907,  xi,  281. 

8  Loc.  cit.  9  Arch,  del  anat.  path,  ct  sc.  affini,  1906. 
"  Deut.  Klinik,  1903-07,  iv,  250. 

11  Beitr.  z.  path.  Anat.  u.  z.  allg.  Path.,  1908,  xliii,  438. 


BRONCHITIS  OBLITERANS  75 

terminations  of  the  bronchi  with  relatively  little  change  other  than 
emphysema  in  the  lung  tissue  itself.  On  section  the  lung  presents  an 
appearance  very  similar  to  that  with  miliary  tuberculosis  from  the 
presence  of  numerous,  grayish-white,  hard,  slightly  projecting  nodules 
about  the  size  of  miliary  tubercles,  from  which  they  differ,  however, 
in  their  angular  or  stellate  form  as  seen  with  the  hand  lens,  and  their 
connection  with  the  small  bronchi  of  which  they  may  be  found  on 
dissection  to  form  the  termination.  On  microscopic  examination  the 
bronchial  lumen  in  the  affected  regions  is  partly  or  wholly  occluded 
by  an  ingrowth  of  connective  tissue,  which  apparently  takes  its  origin 
from  the  bronchial  wall.  Partial  destruction  of  the  epithelium  prob- 
ably precedes  the  new  formation  of  tissue  and  proliferation  of  the 
membrana  propria  and  peribronchial  tissue  with  rupture  of  the  elastic 
coat  accounts  for  the  invasion  of  the  bronchial  lumen.  Connective- 
tissue  invasion  is  also  observed  in  the  neighboring  alveoli,  with  the 
formation  of  Lange's  "miliary  indurative  pneumonia."  Galdi1  has 
described  the  case  of  an  engraver  of  music  with  nodular  induration 
of  isolated  groups  of  alveoli,  loss  of  epithelium  and  inflammatory 
thickening  of  the  terminal  bronchioli,  but  without  invasion  of  the  lumen 
by  connective  tissue.  This  case  does  not  belong  in  this  group,  but  may 
indicate  the  varying  results  of  injury  of  the  tissue  by  different  agents. 

Symptoms. — In  Frankel's  first  case  in  which  the  condition  followed 
the  inhalation  of  the  fumes  of  nitrous  acid,  there  was  an  initial  irrita- 
tive stage  with  severe  dyspnea,  acute  emphysema,  and  widespread 
crepitant  rales,  but  no  outspoken  dulness.  The  first  stage  was  the 
result  of  the  corrosive  action  on  the  bronchial  wall  with  resulting 
hyperemia,  loss  of  the  protecting  epithelium,  and  serous  exudation 
into  the  lumen.  This  was  followed  by  a  period  of  complete  relief  of 
symptoms  and  a  condition  of  well-being  coincident  with  the  subsi- 
dence of  the  inflammatory  exudation.  With  the  development  of  con- 
nective tissue  and  obliteration  of  the  bronchioles  there  was  a  return 
of  the  earlier  symptoms  on  the  fourteenth  day,  and  death  occurred 
six  days  later.  A  similar  clinical  course  was  observed  in  Edens'  first 
case  following  the  inhalation  of  the  fumes  of  nitrous  acid  with  chlorin 
and  with  death  on  the  twenty-sixth  day.  In  his  second  case,  in  which 
the  condition  likewise  followed  the  inhalation  of  nitrous  acid  with 
chlorin  and  in  his  third  case  after  inhalation  of  ammonia  gas  the  initial 
acute  symptoms  subsided  and  the  patients  recovered.  Clinical  data 
are  lacking  or  not  characteristic  in  other  reported  cases. 

Diagnosis. — This  was  made  during  life  and  later  established  at 
postmortem  examination  in  two  of  Frankel's  four  cases  and  in  Edens' 
first  case.  The  disease  resembles  acute  miliary  tuberculosis  from  the 
presence  of  cyanosis,  dyspnea,  emphysema,  and  crepitant  rales  over 
both  lungs,  and  the  absence  of  dulness,  but  may  be  differentiated  by 
the  history,  evidences  on  examination  of  tuberculosis  in  the  lung  or 

1  Deut.  Arch.  f.  klin.  Med.,  Bd.  lxxv,  p.  239. 


76  DISEASES  OF  THE  BRONCHI 

other  parts  of  the  body,  including  a  search  for  choroidal  tubercles 
and  the  finding  of  tubercle  bacilli  in  the  sputum.  Widespread  capil- 
lary bronchitis  with  bronchopneumonia  a*  a  result  of  bronchopul- 
monary infection  may  present  closely  similar  clinical  features.  An 
unusual  degree  of  pulmonary  inflation  may  suggest  the  possibility  of 
an  obliterative  bronchiolitis,  developing  in  the  course  of  such  a  con- 
dition. •  In  the  circumscribed  forms  of  the  disease  the  clinical  diagnosis 
can  hardly  be  made. 

Prognosis. — This  is  grave  as  might  be  expected  from  the  clinical 
and  anatomic  features.  The  condition  even  when  widespread  is 
not  necessarily  fatal,  as  is  indicated  by  the  recovery  of  Edens'  second 
and  third  cases.  The  cases  thus  far  reported  are  too  few  to  admit 
of  safe  prediction  concerning  the  outlook  in  individual  cases.  In 
Edens'  first  case  the  initial  symptoms  were  mild,  and  the  patient  was 
able  to  continue  at  his  work  for  three  weeks  after  the  inhalation  of 
the  acid  fumes.  The  symptoms  then  became  more  intense,  and  he 
died  five  days  later. 

Prophylaxis. — Sufficient  ventilation  should  be  secured  in  rooms 
where  corrosive  fumes  are  generated.  Workers  in  danger  of  the  inhala- 
tion of  acid  or  alkaline  fumes  should  wear  suitable  masks  containing 
a  piece  of  gauze  or  a  sponge  moistened  in  mild  alkaline  or  acid  solution. 

Treatment. — Frankel  recommends  the  inhalation  of  oxygen  when 
there  is  danger  of  suffocation.  At  present  there  are  no  means  of 
checking  the  formation  of  connective  tissue,  and  the  treatment  must 
otherwise  be  that  of  severe  bronchitis  and  bronchopneumonia. 


CHAPTER  V. 
BRONCHITIS. 

1.  ACUTE  TRACHEOBRONCHITIS. 

This  is  the  most  frequent  disturbance  of  the  air  passages,  and  in 
its  milder  forms  a  matter  of  every-day  observation. 

Classification. — The  clinical  features  of  tracheobronchitis  justify 
its  inclusion  among  the  infections.  Its  relation  to  influenza  cannot  be 
regarded  as  settled,  but  certain  etiologic  features  to  be  mentioned 
later  make  it  probable  that  many  if  not  most  of  the  cases  of  tracheo- 
bronchitis occurring  in  the  intervals  between  the  outbreaks  of  pan- 
demic and  endemic-epidemic  influenza  are  to  be  regarded  as  examples 
of  sporadic  influenza.  If  the  influenza  bacillus  be  regarded  as  the  cause 
of  true  influenza,  cases  of  tracheobronchitis  should  be  classed  as  a 
manifestation  of  this  disease  when,  as  occurs  in  a  certain  number  of 
the  cases,  this  organism  is  present,  while  those  cases  with  a  similar 
clinical  picture,  but  in  which  the  influenza  bacillus  cannot  be  found, 
should  be  classed  as  influenza  nostras  or  "la  grippe." 

Etiology. — It  is  difficult  to  present  a  satisfactory  grouping  of  the 
cases  according  to  their  etiology.  A  division  into  cases  due  to  (1) 
infection  and  (2)  mechanical  and  toxic  causes  seems  least  open  to 
objections. 

1.  Infections. — Acute  tracheobronchitis  is  an  infection  of  the  respira- 
tory tract  usually  beginning  in  the  nose  as  a  "cold"  and  proceeding 
downward  with  or  without  involvement  of  the  nasopharynx,  the  ton- 
sils, or  larynx  to  the  deeper  parts  of  the  air  passages.  In  some  cases 
the  process  starts  as  a  disturbance  low  down  in  the  tract  and  extends 
upward,  but  this  is  less  common.  Cases  are  most  numerous  in  the 
colder  months  of  the  year,  and  children  are  much  more  frequently 
affected.  Some  persons  seem  specially  disposed  and  suffer  a  succes- 
sion of  attacks  at  frequent  intervals  during  the  winter.  Group  infec- 
tions are  common  in  the  family  and  among  persons  closely  associated, 
but  the  type  of  the  disturbance  is  likely  to  differ,  appearing  as  a  simple 
rhinitis  in  one,  tonsillitis  in  another,  and  tracheobronchitis  with  or 
without  manifestations  referred  to  the  upper  parts  of  the  tract  in  a 
third.  The  contagiousness  of  such  infections  is  a  matter  of  every-day 
observation,  and  the  disease  develops  following  an  interval  of  only  a 
few  days  after  exposure.  Transmission  from  person  to  person  seems 
more  common  early  in  the  disturbance  and  in  the  presence  of  the  acute 
symptoms. 


78  DISEASES  OF   THE  BRONCHI 

The  use  of  the  term  "cold"  and  its  German  equivalent  "  Erkaltung" 
indicates  a  prevalent  belief  that  chilling  of  the  body  is  an  important 
factor.  It  is  a  common  observation  that  exposure  in  wet  weather, 
sitting  in  wet  clothes  or  in  a  draught,  and  rapid  cooling  of  the  body 
after  perspiring  from  overexertion  precipitate  an  attack,  and  there  is 
some  experimental  evidence  to  show  that  such  indiscretions  may  pro- 
duce abnormal  bronchial  conditions.  Rossbach,1  Midler2  and  others 
have  shown  that  in  animals,  chilling  of  the  body  is  followed  by  a  transi- 
tory increase  of  bronchial  secretion.  In  Midler's  experiments,  atelec- 
tasis in  the  territory  supplied  by  occluded  bronchi,  desquamation  of 
alveolar  epithelium,  and  an  exudate  of  albuminous  fluid  containing 

Fig.  12 


Influenza  bacilli  in  sputum.      X  1000. 

some  fibrin  and  blood  were  also  noted ;  and  it  may  be  that  after  exposure 
to  cold,  conditions  become  more  favorable  for  the  development  of 
organisms  in  the  bronchial  tract  of  an  already  infected  individual. 
While  it  cannot  be  denied  that  exposure  to  cold  and  wet  may  bear 
more  than  a  chance  relation,  yet  it  is  probable  that  its  influence  is 
overestimated.  Many  such  exposures  are  experienced  without  ill 
effects,  and  then  to  the  indiscretion  immediately  preceding  an  infec- 
tion an  unwarranted  importance  is  accorded.  Nansen's  often  quoted 
experience  of  freedom  from  colds  among  the  members  of  his  expedi- 
tion while  exposed  to  the  extremely  low  temperature  of  the  far  North 
and  the  development  of  colds  and  cough  among  many  of  the  party 
when  on  their  return  they  landed  at  a  thickly  inhabited  port,  suggest 
that  exposure  to  cold  alone  is  not  a  sufficient  cause. 

An  important  cause  in  this  group  is  influenza,  the  prevailing  picture 
of  which  in  all  epidemics  has  been  that  of  a  respiratory  infection, 

1  Berl.  klin.  Woch.,  1882.  2  Deut.  Klinik,  1903-04. 


A C  UTE   TEA ClIEOBRONCHI  TIS 


79 


affecting  for  the  most  part  the  upper  parts  of  the  tract  as  a  rhinitis, 
but  in  the  more  severe  cases  extending  to  the  deeper  parts  and  even 
into  the  smallest  branches  of  the  bronchi.    Not  a  year  has  elapsed 


Fig.  13 


Influenza  bacilli  in  alveolar  exudate.      X  1000. 

since  the  great  pandemic  of  1889-90  without  local  outbreaks  in  some 
part  of  the  world.  The  relation  which  isolated  and  small  groups  of 
infection  with  acute  respiratory  symptoms  occurring  in  interepidemic 
periods  bear  to  epidemic  and  pandemic  influenza  is  an  interesting 

Fig.   14 


Culture  of  influenza  bacilli  on  blood-agar  (low  magnification). 

question  which  cannot  yet  be  regarded  as  settled.  It  is  certainly 
reasonable  to  assume  that  in  some  form  the  infecting  organism  in 
epidemic  and  pandemic  influenza  must  be  kept  alive  during  the  inter- 


so 


DISEASES  OF   THE  BRONCHI 


epidemic  period,  and  the  contagious  character  of  and  the  similarity  of 
the  symptoms  in  the  severer  types  of  the  primary  acute  respiratory 
infections  suggest  that  these  and  the  influenza  cases  may  be  due  to  a 
common  cause.  So  far  as  the  influenza  bacillus  is  concerned,  it  must 
be  regarded  as  an  important  infecting  agent  in  a  large  number  of  acute 

Fig.  15 


Smear  preparation  of  influenza  bacilli  from  culture.      X  1000. 

and  chronic  disturbances  during  the  interepidemic  period  and  as  a 
contributing  factor  in  many  other  cases  when  mixed  with  the  pneumo- 
coccus,  pyogenic  cocci,  Micrococcus  catarrhalis,  and  other  organisms. 
The  cases  in  which  it  exists  as  a  practically  pure  infection  present 
no  striking  or  constant  difference  from  the  respiratory  infection  with 

Fig.  16 


Smear  preparation  of  influenza  bacilli  from  culture,  showing  the  occasional  larger  size 
of  the  organisms  and  their  safety-pin  appearance.      X  1000. 


other  organisms  and  without  association  with  influenza  bacilli.  The 
organism  behaves  in  this  respect  like  any  other  of  the  common  respira- 
tory parasites.  In  the  interepidemic  period  the  clinical  diagnosis  of 
"influenza"  often  fails  of  confirmation  by  the  finding  of  influenza 
bacilli  in  the  sputum. 


ACUTE  TRA CHEOBRONCIII TI8 


81 


In  whooping  cough,  invasion  of  the  trachea  and  bronchi  by  the 
Bordet-Gengou  bacillus  is  directly  responsible  for  the  symptoms. 
The  researches  of  Mallory  and  Horner1  indicate  that  a  location  of  the 


Fig.  17 


Bacillus  of  pertussis.     Masses  of  the  bacilli  intimately  associated  with  the  cilia  of   the 
epithelium  of  the  trachea  in  a  case  of  Pertussis.     (Dr.  J.  H.  Wright.) 

Fig.  18 


.-f 


c-^rL  - *  ,  2ft  c 


ics.-» 


-\  :  "    v  r»  J? 


Diphtheroid  bacilli  with  pneumococci  and  influenza  bacilli  in  sputum. 

organisms  between  the  cilia  of  the  epithelial  cells  lining  the  trachea 
and  bronchi  is  apparently  characteristic  of  this  disease  and  probably 


1  Jour.  Med.  Research,  November,  1912, 


82 


DISEASES  OF  THE  BRONCHI 


responsible  for  the  continuous  irritation  which  results  in  coughing 
and  whooping. 

k.s  an  example  of  this  group  measles  may  also  be  mentioned  during 
the  prodromal  stage  of  which  coryza,  redness  of  the  eyes  and  the  lids, 
hyperemia  of  the  mouth  and  throat,  and  catarrh  of  the  trachea  and 
bronchi  are  observed.  Similar  but  less  intense  respiratory  symptoms 
may  be  seen  in  German  measles.  Manifestations  of  secondary  and 
tertiary  syphilis  are  occasionally  noted  in  the  trachea  and  bronchi 
and  are  more  fully  considered  in  another  section.  Tracheobronchial 
catarrh  is  common  in  typhus  fever  and  may  complicate  the  lesions  in  the 
mouth,  pharynx,  and  larynx  of  smallpox.    In  typhoid  fever,  bronchitis 

Fig.  19 


Micrococcus  catarrhalis  colonies  on  agar. 


is  an  early  and  important  symptom,  and  may  so  predominate  in  the 
clinical  picture  as  to  lead  to  an  error  in  diagnosis.  Typhoid  bacilli 
were  cultivated  from  mucopurulent  sputum  without  blood  in  uncom- 
plicated bronchitis  in  typhoid  fever  by  Jehle.1  The  organisms  were 
in  pure  culture  in  one,  mixed  with  diplococci  and  streptococci  in 
another  and  with  influenza  bacilli  in  2  cases.  The  bronchitis  may  be 
due  to  the  typhoid  bacilli  or  other  organisms.  The  development  of  the 
latter  may  be  favored  by  congestion  of  the  mucous  membrane  from 
toxemia  or  hypostasis. 

i  Wien,  kliu,  Woch,,  February  27,  1902. 


ACUTE  TRACHEOBRONCHITIS 


83 


In  diphtheria,  extension  of  the  infection  from  above  may  take  place 
into  the  deeper  parts  of  the  tract.  This  occurs  more  often  when  the 
process  starts  in  the  pharynx  or  larynx  and  from  the  latter  the  lower 
parts  of  the  trachea,  the  larger  and  even  the  finer  bronchi  may  be 
invaded  with  the  formation  of  a  membrane  in  the  affected  regions. 
McPhedran1  refers  to  two  fatal  cases  seen  by  Goldie  without  exudate 
in  the  fauces  and  general  bronchitis  without  membrane  formation. 
Pure  cultures  of  the  diphtheria  bacillus  were  obtained  from  the  secretion. 
The  extension  of  facial  erysipelas  to  the  mucous  membrane  of  the 
mouth  and  pharynx  may  be  followed  by  edema  of  the  glottis,  laryn- 
gitis, tracheitis,  and  bronchitis.  Primary  erysipelas  of  the  larynx 
has  been  described.  Bronchitis  may  also  be  observed  in  connection 
with  variola,  anthrax,  and  glanders.  An  intermittent  bronchitis  has  been 
ascribed  to  malaria,  but  is  not  well  established.  Bronchitis  may 
accompany  plague  pneumonia. 

Fig.  20 


Micrococcus  catarrhalis  in  smear  from  sputum. 

One  of  the  most  common  and  important  causes  is  pulmonary 
tuberculosis  which  is  accompanied  by  acute  catarrhal  inflammation 
of  the  bronchi  leading  to  the  affected  region  in  the  initial  stages  or 
during  an  exacerbation  of  the  localized  forms  of  the  disease  and  a 
diffuse  bronchitis  in  the  pulmonary  form  of  miliary  tuberculosis. 
Involvement  of  the  finer  bronchi  leading  to  the  involved  territory 


1  Osier's  Mod.  Med.,  vol.  iii,  p.  639. 


84  DISEASES  OF  THE  BRONCHI 

is  also  a  constant  accompaniment  of  croupous  pneumonia  and  broncho- 
pneumonia, the  invasion  in  the  former  taking  place  from  below,  and  in 
the  latter  most  often  from  above. 

2.  Mechanical  and  Toxic  Causes. — The  inhalation  of  dust  as  a  carrier 
of  contagious  material  may  be  regarded  as  a  contributing  factor  in 
many  of  the  acute  infections  of  the  bronchi.  In  bronchostenosis  from 
whatever  cause  the  multiplication  of  bacteria  already  present  in  the 
bronchi  or  brought  in  with  an  aspirated  foreign  body  leads  to  inflam- 
mation of  the  bronchi  and  to  the  serious  consequences  referred  to  in  the 
section  under  this  heading.  Following  narcosis  from  ether  inhalation, 
acute  bronchitis  with  or  without  pneumonia  may  be  observed,  and  is 
more  especially  to  be  feared  in  persons  already  subject  to  an  infection 
of  the  respiratory  tract,  the  existing  organisms  probably  finding  con- 
ditions more  favorable  for  development  in  the  increased  bronchial 
secretion.  Of  other  gases,  the  inhalation  of  the  fumes  of  nitrous, 
nitric,  sulphurous  and  hydrochloric  acid,  ammonia  and  chlorin  may  be 
mentioned  as  occasional  causes.  The  internal  administration  of  the 
iodids  may  cause  toxic  symptoms  spoken  of  as  iodism  and  most  often 
manifested  as  a  catarrh  of  the  upper  parts  of  the  tract,  but  at  times 
with  involvement  of  the  lower  passages  and  the  bronchi.  Similar 
though  less  severe  disturbances  may  follow  the  use  of  the  bromids. 
Passive  congestion  of  the  bronchi  is  a  frequent  predisposing  cause 
of  a  type  of  bronchitis  which  may  be  spoken  of  as  a  "stasis  catarrh." 
It  is  commonly  seen  in  the  later  stages  of  broken  cardiac  compensation 
from  whatever  cause,  and  is  doubtless  due  to  the  growth  of  organisms 
always  present  and  ready  to  multiply  under  conditions  favorable  for 
their  development.  Bronchitis  observed  in  the  course  of  chronic 
nephritis  and  obesity  is  probably  also  to  be  ascribed  to  this  cause. 

Bacteriology  of  the  Normal  Respiratory  Tract. — The  presence  of  patho- 
genic organisms  of  varying  degrees  of  virulence  in  the  mouth  in  health 
is  well  established.  Numerous  observations  on  the  deeper  parts  of  the 
tract  have  been  made.  Jundell1  examined  mucus  obtained  from  the 
trachea  after  cocainization  of  the  larynx  and  found  streptococci  and 
a  gonococcus-like  diplococcus  (Micrococcus  catarrhalis  ?)  in  20  of  42 
cases.  In  the  remaining  cases  inoculated  culture  media  remained 
sterile.  Positive  findings  in  the  normal  human  lung  are  recorded  by 
Diirck,2  Beco,3  Kerschensteiner,4  and  Norris  and  Pappenheimer;5 
and  in  the  normal  lung  of  animals  by  Boni6  and  Barthel.7  The  attempt 
to  demonstrate  organisms  was  negative  or  showed  only  a  few  bacteria 
in  the  examinations  of  normal  human  lungs  by  Klipstein,8  Polguere9  and 

1  Baumgarten's  Jahresbericht,  1898,  p.  857. 

2  Deut.  Arch.  f.  klin.  Med.,  vol.  lviii,  p.  368. 

3  Centralbl.  f.  innere  Med.,  1900,  p.  846. 

4  Quoted  from  Miiller,  Deut.  Klinik,  1903-04,  p.  229. 

5  Jour.  Exp.  Med.,  1905,  vol.  vii,  No.  5. 

6  Deut.  Arch.  f.  klin.  Med.,  vol.  lxix. 

7  Centralbl.  f.  Bakt.,  1898,  vol.  xxvi,  No.  11. 

8  Zeit.  f.  klin.  Med.,  vol.  xxxiv- 

9  Des  infections  secondaire,  These  de  Paris,  1888. 


ACUTE  TRACHEOBRONCHITIS  85 

Barthel;1  and  in  the  examination  of  the  lungs  of  animals  by  Hilde- 
brand,2  Beco,3  and  Miiller.4  Kerschensteiner5  had  the  opportunity 
to  examine  the  normal  lungs  of  an  individual  immediately  after  execu- 
tion by  decapitation,  and  found  among  other  organisms  staphylococcus 
albus  and  pseudodiphtheria  bacillus,  but  inoculation  of  mice  with 
material  from  the  lung  failed  to  produce  an  infection.  Norris  and 
Pappenheimer  call  attention  to  the  readiness  with  which  after  death 
bacteria  can  find  ingress  into  the  deeper  parts  of  the  respiratory  tract 
from  the  mouth  and  throat. 

In  spite  of  the  somewhat  conflicting  results  by  different  observers 
the  lower  parts  of  the  air  passages  and  even  the  lungs  can  by  no  means 
be  regarded  as  free  from  bacteria  even  in  health,  and  their  presence 
may  in  large  measure  be  ascribed  to  the  inhalation  of  infected  dust. 
The  infrequency  with  which  infection  occurs  in  spite  of  the  prevalence 
of  bacteria  is  due  to  the  passage  of  air  through  a  sinuous  channel  on 
its  way  to  the  deeper  parts  of  the  tract,  the  protective  action  of  ciliary 
motion  constantly  tending  to  drive  small  particles  outward,  the 
barrier  offered  by  a  surface  layer  of  mucus  and  epithelium  against 
penetration  into  the  tissue,  the  defensive  action  of  phagocytes,  and 
expulsion  by  cough  of  larger  particles  of  foreign  material. 

Bacteriology  of  the  Sputum  with  Bronchitis. — Numerous  observations 
have  shown  that  in  the  majority  of  cases  the  influenza  bacillus,  the 
pneumococcus,  the  pyogenic  cocci,  the  staphylococcus,  the  Micrococcus 
catarrhalis,  and  less  commonly  other  pathogenic  organisms  may  be 
found  in  the  sputum  singly  or  combined  in  the  specimens.  It  is  the 
general  experience  that  material  from  the  upper  parts  of  the  tract 
contains  a  great  variety  of  organisms,  and  the  examination  of  carefully 
selected  and  washed  purulent  particles  from  below  more  often  discloses 
only  one  or  possibly  two  organisms  as  the  apparent  cause  of  the  process. 
Workers  at  different  times  and  in  different  places  have  found  now  one 
and  then  another  organism  predominating  in  the  specimens. 

In  1892  Pfeiffer5  published  his  discovery  of  the  influenza  bacillus,  and 
this  was  followed  in  18937  by  his  more  elaborate  report.  This  organism 
was  found  in  all  the  uncomplicated  cases  of  influenza  in  pure  culture 
in  the  sputum  and  regarded  as  the  cause  of  the  disease.  Contrary  to 
Pfeiffer's  observations  it  has  since  been  found  in  interepidemic  periods, 
with  or  without  influenza,  by  a  great  many  investigators.  Between 
August,  1902,  and  January,  1904,  I8  examined  186  sputa  from  patients 
suffering  from  acute  or  chronic  disease  of  the  respiratory  tract,  for  the 
most  part  bronchitis.  In  110  (59  per  cent.)  organisms  having  the 
morphology  and  staining  reaction  of  influenza  bacilli  were  found  in 

1  Loc.  cit.  2  Ziegler's  Beitrage,  vol.  ii,  p.  143. 

s  Loc.  cit.  4  Deut.  Arch.  f.  klin.  Med.,  vol.  lxxi,  p.  513. 

6  Loc.  cit.  6  Deut.  med.  Woch.,  1892,  ii,  28. 

7  Zeit.  f.  Hyg.,  1893,  vol.  xiii. 

8  Infections  of  the  Respiratory  Tract  with  Influenza  Bacilli  and  Other  Organisms, 
their  Clinical  and  Pathological  Similarity  and  Confusion  with  Tuberculosis,  Boston 
Med.  and  Surg.  Jour.,  May  11  and  18,  1905. 


86  DISEASES  OF  THE  BRONCHI 

varying  numbers.  In  5G  (30  per  cent.)  the  organisms  were  shown  by 
culture  to  conform  in  all  respects  to  Pfeifi'er's  influenza  bacillus,  and 
in  47  (25  per  cent.)  they  were  in  overwhelming  numbers.  Organisms 
resembling  pneumococci  were  found  in  70  per  cent,  of  the  cases,  but 
were  represented  as  a  pure  infection  in  only  eight.  The  Micrococcus 
catarrhalis  was  found  as  a  practically  pure  infection  in  5  cases.  Ghon, 
Pfeiffer,  and  Sederl1  found  the  Micrococcus  catarrhalis  alone  or  mixed 
with  pneumococci,  influenza  bacilli,  staphylococci  and  streptococci 
in  many  cases  of  acute  or  subacute  bronchitis  and  bronchopneumonia. 
Frankel2  found  pneumococci  and  streptococci  most  often  in  acute 
bronchitis.  Marfan,3  Duflocq  and  Menetrier,4  Bartel,5  and  Jundell'5 
found  the  pneumococcus  in  acute  bronchitis.  In  children,  Holt7 
found  Staphylococcus  aureus,  pneumococcus,  the  influenza  bacillus, 
and  the  streptococcus  in  the  bronchial  secretion  of  children  with 
bronchitis.  The  occasional  presence  of  Friedliinder's  bacillus,  Micro- 
coccus tetragenus,  and  the  colon  bacillus  is  noted  by  various 
observers. 

These  and  numerous  other  investigations  have  shown  that  there  is 
little  uniformity  in  the  bacteriologic  findings.  Mixed  infections  are 
the  rule,  and  one  organism  as  a  practically  pure  and  persistent  infec- 
tion the  exception.  One  group  may  be  found  to  predominate  in  the 
first  examination,  but  subsequent  investigation  of  the  sputum  from 
the  same  case  frequently  shows  that  contaminations  have  taken  place, 
and  since  no  sharp  distinction  can  be  drawn  between  the  pathogenic 
power  of  different  organisms  found  in  the  sputum  the  observer  must 
remain  in  doubt  as  to  the  relative  importance  of  any  one  infecting 
group. 

It  should  be  noted  that  these  common  respiratory  organisms  occur 
in  all  forms  of  bronchitis.  They  may  be  found  in  the  sputum  in  the 
bronchitis  following  a  "cold,"  influenza,  wdiooping  cough,  measles, 
typhoid  fever,  diphtheria,  tuberculosis  and  pneumonia.  They  occur 
as  the  apparent  sole  cause  in  the  bronchitis  of  "cold"  and  influenza,  but 
are  now  recognized  as  secondary  invaders  in  the  more  specific  infections. 
They  uniformly  appear  also  in  the  bronchitis  due  to  mechanical  and 
toxic  causes.  The  suggestion  is  obvious  that  they  cannot  fairly  be 
regarded  as  an  adequate  cause  of  either  the  bronchitis  of  "cold"  or 
influenza,  but  that  in  these  as  well  in  all  other  forms  of  bronchitis  they 
are  rather  to  be  regarded  as  secondary  invaders.  The  independent 
position  so  long  occupied  by  the  influenza  bacillus  is  largely  discredited 
by  its  constant  appearance  in  company  with  other  common  parasites, 
and  it  is  no  longer  to  be  regarded  as  in  good  standing  as  a  cause  of 

1  Zeit.  f.  klin.  Med.,  1902,  vol.  xliv. 

2  Spec.  Path.  u.  Ther.  d.  Lungenkrankheiten,  1904,  p.  141. 

3  Traite  de  med.  Charcot,  Bouchard,  Brissaud,  T.  iv,  p.  296. 

4  Arch.  gen.  de  med.,  1890,  1894,  and  1895. 

*  Centralbl.  f.  Bakt.,  Abth.  i,  Bd.  xxiv,  p.  401. 

6  Baumgarten's  Jahresber.,  1898,  p.  857. 

7  Jour.  Amer.  Med.  Assoc,  October  8,  1910. 


ACUTE  TRACHEOBRONCHITIS  87 

influenza,  which  is  probably  due  to  another  and  as  yet  undiscovered 
cause. 

Correlation  of  the  Bacteriologic  Findings  with  the  Clinical  Picture. — 
An  attempt  has  often  been  made  to  separate  the  cases  into  clinical 
groups  according  to  the  type  of  the  bacterial  infection.  After  the 
exclusion  of  cases  showing  mixed  cultures,  examples  of  single  infections 
are  so  uncommon,  even  in  large  series,  that  only  a  small  group  is  left 
for  comparison,  and  in  these  the  symptoms  of  onset,  the  course  and 
duration  do  not  seem  to  be  distinctive.  The  amount  of  prostration 
may  be  as  great  in  one  as  in  the  other,  and  all  tend  to  set  up  diffuse 
or  local  bronchitis  and  a  varying  degree  of  bronchopneumonia. 

Pathology. — Opportunities  for  postmortem  examination  of  simple 
and  uncomplicated  bronchitis  are  exceptional  owing  to  the  infrequency 
of  a  fatal  termination,  and  our  knowledge  of  the  changes  is  for  the  most 
part  the  result  of  autopsies  made  on  patients  dying  with  broncho- 
pneumonia. In  a  few  instances  the  gross  appearance  has  been  studied 
during  life  with  the  bronchoscope. 

The  mucous  membrane  is  reddened,  injected  and  swollen,  and  its 
surface  is  the  site  of  a  mucoid,  mucopurulent  or  purulent  exudation. 
Inflammatory  swelling  of  the  smaller  bronchi  may  lead  to  closure  of  the 
lumen  and  to  atelectasis  of  the  corresponding  pulmonary  region.  This 
is  much  more  common  in  children  owing  to  the  narrowness  of  the 
passages.  Enphysema  of  parts  of  the  lung  not  involved  with  broncho- 
pneumonia may  also  be  observed. 

Bronchoscopic  inspection  of  the  changes  in  the  smaller  bronchi 
during  life  have  been  made,  among  others  by  Schrotter,1  and  offers  an 
explanation  of  the  mechanical  relations  during  inspiration  and  expira- 
tion. If  the  mucous  membrane  is  only  moderately  swollen  and  the 
lumen  still  patent,  inspiratory  enlargement  and  expiratory  narrowing 
of  the  passages  can  usually  be  observed.  Even  with  apparent  total 
occlusion  of  the  bronchus,  a  quick  forcible  inspiration  may  open  the 
lumen.  Involvement  of  a  large  number  of  bronchi  may  considerably 
obstruct  the  inspiratory  current  of  air,  and  the  greater  narrowing 
of  an  already  contracted  lumen  during  expiration  will  still  further 
impede  and  delay  the  outgoing  current.  During  forcible  expiration 
with  cough,  the  bronchial  walls  are  everywhere  pressed  together. 
The  bronchial  secretion  is  momentarily  held  back  and  then  moves 
upward  with  the  sudden  relief  of  the  obstruction. 

On  microscopic  examination  of  the  acutely  inflamed  larger  bronchi, 
swelling  and  degenerative  changes  may  be  observed  in  the  ciliated 
epithelial  cells.  The  epithelial  layer  and  the  tunica  propria,  and  in 
severe  grades  of  inflammation,  even  the  muscular  fibers,  the  mucous 
glands,  the  neighborhood  of  the  cartilages  and  the  fibro-elastic  tunic 
are  infiltrated  with  polymorphonuclear  leukocytes.  Desquamation 
of  the  epithelium  takes  place.    The  capillaries  of  the  tunica  propria 

1  Klinik  der  Bronchoskopie,  1906,  p.  184. 


88  DISEASES  OF  THE  BRONCHI 

are  swollen  and  engorged  with  blood.  The  mucous  "'lands  "of  the 
bronchial  wall  arc  in  a  condition  of  active  secretion  and  drops  of  mucus 
or  mucopus  may  be  found  protruding  from  the  orifices  of  their  excre- 
tory ducts.  Midler1  found  the  goblet  cells  not  only  of  the  larger, 
but  also  of  the' medium  and  finer  bronchi,  increased  in  number  on 
comparison  with  preparations  from  normal  bronchi.  The  abundance 
of  mucus  is  to  be  ascribed  to  increased  activity  of  the  mucous  glands 
and  proliferation  of  the  goblet  cells. 

Symptoms. — Prodromata  are  usually  lacking.  The  attack  commonly 
begins  as  a  "cold"  in  the  nose  or  as  a  sore  throat.  In  children  the 
adenoid  tissue  in  the  nasopharynx  is  frequently  the  starting-point  of  the 
infection.  At  the  onset  there  is  chill  or  chilliness,  headache,  malaise, 
general  pains,  loss  of  appetite,  and  slight  elevation  of  temperature. 
The  fever  seldom  rises  above  101°  to  102°  in  adults,  but  may  be  higher 
in  children.  All  parts  of  the  tract  may  be  involved  in  the  course  of  a 
day  or  two  by  extension  downward,  or  the  tracheobronchial  region 
may  be  primarily  invaded.  Attacks  vary  in  the  intensity  and  extent 
of  the  tracheobronchial  manifestations.  The  disturbance  may  be 
limited  to  the  trachea  and  larger  bronchi,  involve  as  well  the  medium 
and  smaller  passages  or  extend  to  the  bronchioles  and  the  lung. 

The  first  intimation  of  the  tracheobronchial  involvement  is  usually 
a  sensation  of  persistent  tickling  or  irritation  in  the  cervical  and  sub- 
sternal course  of  the  trachea,  and  this  may  be  increased  by  tracheal 
pressure  or  extension  of  the  head,  putting  the  trachea  on  the  stretch. 
Implication  of  the  larynx  may  be  indicated  by  hoarseness  or  aphonia. 

Cough  begins  at  once,  and  is  usually  constant,  harassing,  and  without 
expectoration.  At  this  stage  it  is  largely  reflex  and  due  to  the  irrita- 
tion of  the  trachea  and  bronchi,  the  most  sensitive  parts  of  which  are 
the  posterior  walls  and  the  regions  just  below  the  glottis  and  the  tracheal 
bifurcation.  It  may  be  paroxysmal,  and  in  children,  spasmodic  par- 
tial closure  of  the  glottis  may  give  rise  to  a  stridulous  inspiratory 
sound  resembling  the  whoop  in  whooping  cough.  The  cough  is  aggra- 
vated by  talking,  crying,  excitement  or  change  of  temperature,  and  is 
likely  to  be  worse  at  night,  perhaps  because  of  restricted  expansion 
of  parts  of  the  lung  and  a  tendency  of  accumulated  secretion  to  irri- 
tate the  more  sensitive  posterior  regions  in  the  prone  position.  The 
lung  itself  is  insensitive  and  lesions  here  do  not  excite  cough.  In 
conditions  of  extreme  weakness  or  somnolence  cough  may  be  absent. 
In  children  a  severe  attack  of  cough  is  frequently  followed  by  vomiting, 
which  is  seldom  observed  in  other  than  highly  sensitive  adults. 

The  rate  of  respiration  is  usually  unaltered  in  uncomplicated  cases 
beyond  such  acceleration  as  can  be  ascribed  to  the  fever.  A  more 
rapid  rate  suggests  a  pulmonary  complication.  Dyspnea  is  not  ordi- 
narily a  feature  of  uncomplicated  bronchitis  of  the  larger  passages, 
but  is  one  of  the  most  important  symptoms  of  involvement  of  the 

1  Deut.  Klinik,  1903-04,  p.  245/ 


ACUTE  TRACHEOBRONCHITIS  89 

smaller  tubes,  and  its  degree  may  well  be  taken  to  indicate  the  severity 
and  extent  of  the  disturbance.  The  dyspnea  is  both  inspiratory  and 
expiratory,  never  exclusively  inspiratory  as  in  laryngeal  stenosis. 

Moderate  elevation  of  temperature  is  common  during  the  first 
twenty-four  to  forty-eight  hours  of  the  attack,  after  which  it  usually 
falls  to  normal  even  though  the  cough  and  expectoration  continue. 
Persistence  of  fever  without  abatement  for  longer  than  two  to  three 
days,  or  an  elevation  following  a  previous  decline,  suggests  a  complica- 
tion with  the  chances  in  favor  of  bronchopneumonia.  The  fall  in  the 
temperature  is  usually  by  lysis.  The  pulse  is  elevated  in  proportion 
to  the  fever. 

Pain  is  not  ordinarily  a  feature,  but  for  some  days  after  an  attack 
during  which  there  has  been  much  irritative  cough,  the  lower  parts 
of  the  chest  and  the  epigastrium  may  be  painful,  with  deep  inspiration 
and  cough,  and  tender  on  pressure  in  consequence  of  muscular  strain. 

Digestive  disturbances  are  usually  limited  to  anorexia  in  adults  and 
vomiting  in  children.  During  the  attack  the  tongue  may  be  coated. 
Some  loss  of  weight  and  strength  are  common.  Sputum  may  be 
obtained  with  difficulty  or  not  at  all  in  children,  the  aged,  and  in  ex- 
treme adynamia  from  any  cause.  It  is  usually  then  swallowed  and 
not  expectorated.  It  is  at  first  mucoid  (sputum  crudum)  and  scanty, 
but  soon  becomes  mixed  with  small  white  or  yellowish  streaks  and 
masses  of  purulent  material,  and  is  then  spoken  of  as  mucopurulent 
(sputum  coctum).  As  the  disturbance  progresses,  and  frequently 
after  the  subsidence  of  the  acute  symptoms,  it  becomes  more  and  more 
purulent  and  yellowish  or  yellowish  green  in  color.  It  is  seldom  abun- 
dant in  uncomplicated  cases  unless  the  bronchial  involvement  has  been 
severe  and  extensive.  Gradually  diminishing  cough  and  expectora- 
tion may  outlast  the  acute  symptoms  for  several  weeks.  The  sputum 
may  be  blood-streaked  or  faintly  blood-tinged,  but  frank  admixture 
with  blood  is  uncommon  with  simple  bronchitis  and  bronchopneumonia, 
and  the  rusty  tenacious  sputum  of  croupous  pneumonia  is  almost 
never  seen.  Microscopic  examination  of  the  mucoid  sputum  of  the 
early  period  shows  oftentimes  an  abundance  of  ciliated  epithelial 
cells,  occasional  red-blood  corpuscles,  and  a  few  large  epithelial  cells 
with  vacuolated  single  nucleus  and  pigment-containing  protoplasm. 
As  the  sputum  becomes  more  purulent,  the  number  of  pus  cells  increase 
and  the  ciliated  epithelial  cells  diminish  or  disappear.  The  bacterio- 
logic  findings  have  already  been  described. 

Signs. — There  are  no  physical  signs  in  the  milder  cases  with  involve- 
ment alone  of  the  trachea  and  primary  bronchi. 

Inspection  is  usually  negative,  but  diminished  inspiratory  expansion 
of  the  affected  side  may  be  observed  with  unilateral  bronchitis  and 
cyanosis,  rapid  and  superficial  breathing  and  dyspnea  with  extensive 
bilateral  involvement  of  the  finer  passages.  Inspiratory  depression 
of  the  lower  sternal  and  lateral  aspects  of  the  chest  may  also  be  noted. 
On  percussion  there  are  no  changes  with  the  exception  of  circumscribed 


90  DISEASES  OF  THE  BRONCHI 

dulness  with  atelectasis  or  hyperresonance  with  emphysema.  On 
palpation  delayed  inspiratory  motion  of  an  affected  region  and  coarse 
rales  may  be  felt. 

The  most  important  and  often  the  only  evidence  of  bronchitis  is 
obtained  on  auscultation,  by  means  of  which  the  distribution  in  respect 
to  the  various  parts  or  the  whole  of  both  lungs  and  the  size  of  the 
affected  tubes  may  be  determined.  Auscultation  is  usually  negative 
when  the  disturbance  is  limited  to  the  trachea  and  primary  bronchi, 
but  coarse,  sonorous  sounds  over  both  lungs  may  be  due  to  secretion 
in  the  trachea  or  at  the  tracheal  bifurcation. 

Inflammation  of  the  medium  and  smaller  bronchi  may  be  indicated 
at  first,  while  there  is  swelling  of  the  mucous  membrane  without  any 
considerable  amount  of  fluid  by  dry  rales  of  a  sonorous  or  sibilant 
quality.  The  rales  are  due  to  the  vibration  of  viscid  secretion  lining 
the  wall  or  traversing  the  lumen  of  the  passage  or  to  the  motion  of 
air  through  the  narrowed  channels.  The  sonorous  rales  usually  arise 
in  the  larger  and  the  sibilant  rales  in  the  smaller  bronchi.  They  are 
commonly  of  about  equal  intensity  over  both  lungs,  and  may  be 
audible  to  the  patient  as  well  as  the  examiner  or  even  at  a  distance. 

Later  in  the  course  of  the  disease,  moist  non-consonating  rales  appear 
during  both  inspiration  and  expiration.  They  are  due  to  the  bubbling 
of  air  through  fluid  in  the  bronchi  and  are  coarse,  medium  or  fine, 
according  to  the  size  of  the  affected  passage.  They  are  to  be 
distinguished  by  their  less  clear-cut,  sharp  and  distinct  quality  from 
the  moist  consonating  or  resonant  rales  which  arise  in  bronchi  sur- 
rounded by  consolidated  pulmonary  tissue,  a  distinction  which  is 
important  but  not  always  easily  made.  Fine  non-consonating  moist 
rales  may  be  distinguished  from  fine  crepitation  heard  at  times  during 
deep  inspiration  at  the  pulmonary  margin  of  persons  in  health,  and 
over  atelectatic  areas  by  the  smaller  size  of  the  latter  and  their 
disappearance  after  repeated  deep  breathing  or  cough.  Moist  non- 
consonating  rales  may  be  evenly  distributed  over  all  parts  of  the  chest, 
but  are  usually  more  numerous  at  the  bases  in  uncomplicated  bronchitis. 
It  is  important  to  determine  and  record  their  distribution,  which  is 
often  variable  in  successive  examinations.  The  posterior  and  lower 
parts  of  the  chest  are  most  often  affected.  It  may  be  stated  as  a 
general  rule  that  whether  non-consonating  or  consonating,  the  persistence 
of  rales  over  any  one  place  in  the  lung  is  evidence  not  of  bronchitis 
alone,  but  of  invasion  of  the  pulmonary  tissue  in  the  region  in  question, 
even  without  other  evidence  of  involvement  of  the  lung.  Persistence 
of  rales  at  the  apices  almost  invariably  indicates  pulmonary  tuberculosis, 
but  may  be  due  to  other  causes. 

Changes  in  the  character  of  the  breathing  may  be  noted.  A  dimin- 
ished respiratory  murmur  over  regions  supplied  by  the  involved  bronchi 
is  common  and  due  to  diminished  ingress  and  egress  of  air  through  the 
narrowed  channels.  At  times,  especially  in  infants  and  young  children, 
the  breath  sounds  may  be  absent  in  consequence  of  complete  occlusion 


ACUTE  TRACHEOBRONCHITIS  91 

of  the  tubes  and  atelectasis  of  the  corresponding  territory.  If  the 
patient  is  asked  to  breathe  deeply  or  cough,  the  dislodgement  or 
removal  of  secretion  may  be  followed  by  normal  breathing.  Another 
change  of  frequent  occurrence  is  a  prolongation  of  expiration  which 
arises  in  consequence  of  the  greater  narrowing  of  an  already  contracted 
lumen  and  delay  of  the  outgoing  current  of  air  during  this  phase  of 
respiration.  Rough  or  uneven  inspiration  is  occasionally  heard  and 
may  be  ascribed  to  variation  in  the  caliber  of  the  bronchi  from  adherent 
secretion.  Cog-wheel  breathing  may  also  be  heard.  In  some  cases 
the  rales  are  so  loud  or  abundant  as  to  make  the  respiratory  murmur 
inaudible. 

Complications. — The  acute  infections  of  the  respiratory  tract  are 
not  infrequently  complicated  by  otitis  media  and  at  times  by  involve- 
ment of  the  accessory  nasal  sinuses.  But  the  most  common  complica- 
tion is  bronchopneumonia  which  invariably  accompanies  capillary 
bronchitis  and  is  frequent  in  the  more  severe  types  of  infection  involv- 
ing the  medium  and  smaller  bronchi.  Acute  bronchiectasis  may 
develop  in  consequence  of  the  bronchopulmonary  infection.  When 
pleuritis  is  observed  in  the  course  of  bronchitis,  a  complicating  broncho- 
pneumonia is  also  likely  to  be  present. 

Diagnosis. — The  onset  with  catarrhal  symptoms  in  the  nose  and 
throat  followed  by  a  sense  of  irritation  along  the  course  of  the  trachea 
and  cough  and  expectoration  running  a  mild  and  short  course  are  the 
chief  clinical  features.  The  absence  of  physical  signs  on  examination 
of  the  chest  is  to  be  expected  when  only  the  trachea  and  primary 
bronchi  are  involved.  The  secretion  from  nasopharyngeal  catarrh 
may  be  expectorated  by  cough,  and  in  doubtful  cases  an  inspection 
of  these  regions  and  the  trachea  will  be  helpful.  Laryngoscopic  exami- 
nation and  the  finding  of  redness  and  secretion  in  the  trachea  may  be 
needed  to  establish  the  deeper  parts  of  the  tract  as  the  source  of  the 
expectorated  material.  The  presence  of  rales  is  confirmatory,  and 
from  their  character  and  distribution  certain  deductions,  already 
discussed,  may  be  drawn  concerning  the  parts  of  the  bronchial  tree 
affected. 

For  the  present  there  are  no  means  of  differentiating  the  simple 
infections  which  start  as  a  "cold"  from  cases  of  sporadic  influenza, 
and  no  clinical  distinction  can  be  made  between  infection  with  the 
pneumococcus,  the  pyogenic  cocci,  the  influenza  bacillus  and  the 
Micrococcus  catarrhalis,  singly  or  combined.  Measles  should  be  con- 
sidered in  the  presence  of  an  acute  infection  of  the  upper  respiratory 
tract,  and  may  be  suggested  by  a  history  of  exposure,  the  presence  of 
oculonasal  catarrh,  and  the  discovery  of  Koplik's  spots  before  the 
rash  appears.  Whooping  cough  may  be  simulated  in  children  with 
paroxysmal  cough,  accompanied  by  cyanosis  and  dyspnea  and  ter- 
minating in  an  attack  of  vomiting,  but  the  characteristic  inspiratory 
whoop  is  lacking  in  the  simpler  infections.  Tracheobronchitis  occur- 
ring in  the  course  of  typhoid,  should  be  suspected  when  the  fever 


92  DISEASES  OF  THE  BRONCHI 

persists  longer  than  a  few  days  and  may  be  established  early  by  blood- 
cultures,  investigation  of  the  urine  and  stool  for  typhoid  bacilli,  and 
later  by  rose  spots, enlargement  of  the  spleen  and  positive  Widal  test. 
There  are  eases  of  syphilis  in  which  tracheobronchial  catarrh  is  a 
prominent  symptom  during  the  secondary  and  tertiary  period,  and  if 
this  disease  cannot  be  otherwise  excluded  a  Wassermann  test  should 
be  made.  Bronchostenosis  should  be  considered  in  cases  without 
preceding  catarrhal  symptoms  in  the  nose  or  throat  and  with  par- 
oxysmal cough  and  dyspnea. 

An  acute  bronchitis  may  precede  or  accompany  croupous  pneumonia, 
and  twenty-four  to  forty-eight  hours  may  elapse  from  the  beginning 
of  the  latter  without  evidence  of  pulmonary  consolidation  on  physical 
examination.  If  the  initial  chill  and  pain  in  the  side  are  absent,  the 
pneumonia  may  not  be  suspected.  High  and  persistent  fever,  marked 
toxic  symptoms  and  rusty  sputum  occurring  in  what  seems  a  simple 
bronchitis  should  suggest  croupous  pneumonia  even  in  the  absence  of 
other  signs  which  are  likely  to  appear  later. 

Infection  of  the  deeper  parts  of  the  bronchial  tract  is  likely  to  be 
followed  by  bronchopneumonia  of  which  there  may  be  little  or  no 
evidence  on  physical  examination.  The  differentiation  between  early 
pulmonary  invasion  with  the  tubercle  bacillus  and  the  more  per- 
sistent types  of  infection  with  other  organisms  considered  in  this 
section,  is  an  ever-present  difficulty  which  cannot  be  resolved  by 
the  absence  of  tubercle  bacilli  and  the  finding  of  other  organisms 
in  the  expectoration.  The  distinguishing  features  of  bronchitis,  simple 
bronchopneumonia,  and  pulmonary  tuberculosis  are  contrasted  in  the 
section  on  Bronchopneumonia. 

Examination  of  the  sputum  is  important,  and  material  may  be 
obtained  in  children  by  exciting  a  cough  by  irritation  of  the  pharynx 
and  catching  the  resulting  expectoration  on  a  swab.  Bacteriologic 
examination  so  far  as  the  common  organisms  is  concerned,  is  rather 
of  academic  than  of  practical  interest,  but  should  be  made  for  the 
purpose  of  finding  tubercle  bacilli,  the  diphtheria  bacillus  or  other 
specific  organisms. 

Course  and  Prognosis. — In  primary  tracheobronchitis  the  prognosis 
is  good,  and  the  acute  symptoms  are  commonly  over  in  the  course  of 
a  few  days,  but  the  cough  and  expectoration  usually  continue  with 
diminishing  severity  for  a  period  of  from  ten  days  to  two  weeks  or 
longer.  In  infants  and  young  children  and  in  the  aged,  or  in  those 
already  gravely  ill  from  another  cause,  the  outlook  is  less  hopeful, 
largely  owing  to  the  frequency  with  which  bronchopneumonia  arises 
as  a  complication.  Even  in  healthy  adults  there  is  a  tendency  of  the 
severe  infections  to  end  in  permanent  damage  to  the  pulmonary  sub- 
stance, but  such  a  termination  is  also  to  be  ascribed  to  bronchopneu- 
monia. In  patients  already  subject  to  infection  with  the  tubercle 
bacillus,  a  previously  inactive  or  slowly  advancing  tuberculous  lesion 
may  be  excited  to  more  rapid  progress. 


ACUTE  TRACHEOBRONCHITIS  93 

Prophylaxis. — In  view  of  the  contagiousness  of  the  acute  respira- 
tory infections,  isolation  should  be  practised  when  possible,  and  the 
patient  and  family  instructed  concerning  measures  of  protection. 
The  sputum  should  not  be  allowed  to  dry,  but  should  be  expectorated 
carefully  into  a  special  receptacle  without  soiling  the  beard  or  mous- 
tache. If  the  patient  coughs  or  sneezes,  expelled  particles  of  sputum 
should  be  caught  in  a  piece  of  cloth  placed  in  front  of  the  mouth. 
Soiled  cloths  may  be  placed  in  a  paper  bag  pinned  to  the  bed  and  later 
burned  or  washed  after  boiling.  The  fingers  should  not  be  moistened 
in  the  mouth  in  turning  the  leaves  of  books,  public  documents,  etc. 
Soiled  bed  and  body  linen  should  be  boiled  before  being  sent  to  the 
laundry.  Thermometers  and  table  utensils  should  be  kept  separate. 
Dusting  should  be  done  with  a  damp  cloth  and  sweeping  with 
a  damp  broom.  An  infected  individual  should  sleep  alone.  An 
abundance  of  sunlight  and  fresh  air  limit  the  danger  of  contagion. 
Expectorated  material  should  be  burned.  These  and  other  recom- 
mendations similar  to  those  applicable  to  the  prevention  of  pulmonary 
tuberculosis  may  be  made  for  the  simpler  respiratory  infections. 

Persons  subject  to  repeated  attacks  of  acute  respiratory  infection 
should  be  especially  careful  to  avoid  exposure  to  wet  and  cold.  Some 
protection  may  be  afforded  by  thin  woolen  underwear  and  such  efforts 
at  increasing  resistance  as  sleeping  with  the  window  open,  spending 
much  time  in  the  open  air,  and  cool  morning  baths  followed  by  friction. 
A  good  reaction  should  follow  the  bath.  It  is  well  to  begin  the  harden- 
ing process  in  warm  weather.  Enlarged  tonsils  and  adenoids  may 
be  the  starting  point  of  the  infection,  and  if  so,  their  removal  should 
be  considered. 

Treatment. — There  is  no  specific  treatment.  In  the  majority  of 
cases  the  disease  runs  its  course  quite  independent  of  attempted 
relief.  The  most  important  measures  are  those  undertaken  to  spare 
the  strength  of  the  patient  and  alleviate  symptoms. 

Even  the  mild  cases  should  be  regarded  as  serious  because  of  the 
proximity  of  the  infection  to  the  lung,  and  the  patient  should  be  con- 
fined to  the  house  and  the  bed  and  remain  there  until  the  acute  symp- 
toms and  fever  have  subsided.  A  milder  and  shorter  course  with  less 
danger  of  complications  may  be  expected  when  this  is  done.  Smoking 
should  not  be  allowed  and  conversation  should  be  reduced  to  a  mini- 
mum. At  the  onset  the  patient  may  take  a  hot  bath  and  then  get  to 
bed  between  warmed  blankets  with  hot-wTater  bottles  at  the  feet. 
A  drink  of  hot  lemonade  may  start  perspiration  which  often  seems  to 
relieve  the  headache  and  general  pains.  Chilling  of  the  body  may  be 
followed  by  an  aggravation  of  symptoms,  and  cold  should  be  limited  to 
cold  applications  for  the  relief  of  pain. 

There  are  no  special  restrictions  concerning  diet,  and  the  patient 
may  take  as  much  of  light  and  easily  digestible  food  as  he  likes. 

Medicines  are  often  unnecessary,  but  if  the  headache  and  general 
pains  are  distressing,  an  ice-cap  and  Dover's  powder  gr.  10  (0.650 


94  DISEASES  OF  THE  BRONCHI 

gm.)  may  be  ordered.  If  the  bowels  have  not  moved,  a  mild  saline, 
as  sodium  phosphate  gr.  30  (1.950  gms.),  in  a  half-tumbler  of  luke- 
warm water,  may  be  given.  The  eoal-tar  products  should  be  used 
with  caution,  but  if  the  headache  or  general  pains  are  distressing, 
antipyrin  or  phenacetin  gr.  10  (0.650  gm.),  combined  witlwall'ein 
gr.  3  (0.195  gm.),  may  give  relief,  but  their  use  should  not  be  long 
continued.    Aspirin  gr.  10  (0.650  gm.)  may  also  be  tried. 

If  the  patient  is  harassed  by  irritative  and  unproductive  cough 
which  disturbs  his  sleep  and  unnecessarily  taxes  his  strength,  heroin 
gr.  ,V  (0.0054  gm.)  or  morphin  may  be  used.  Cough  is  necessary 
for  the  expulsion  of  secretion  which,  if  it  remains,  may  increase  the 
danger  of  atelectasis  or  aspiration  pneumonia,  and  narcotics  should  not 
be  used  without  such  a  special  indication  and  only  as  a  temporary 
expedient. 

When  a  scanty  and  tenacious  sputum  is  raised  with  difficulty,  a 
stimulating  expectorant  such  as  ammonium  chloride  gr.  10  (0.650  gm.) 
often  seems  to  be  of  great  assistance.  Senega  and  squill  are  at  times 
used,  but  are  less  desirable.  Nauseating  expectorants  such  as  tartar 
emetic,  ipecac,  apomorphine,  etc.,  are  unnecessary  in  simple  bronchitis. 


2.  CAPILLARY   BRONCHITIS. 

Infection  of  the  finer  ramifications  of  the  bronchial  tree  is  always 
accompanied  by  invasion  of  the  adjacent  parts  of  the  lung,  and  it 
therefore  seems  best  to  consider  capillary  bronchitis  in  connection 
with  bronchopneumonia. 


3.  CHRONIC   BRONCHITIS. 

This  is  usually  to  be  regarded  as  a  symptom  of  some  more  important 
and  more  serious  underlying  disease  rather  than  as  an  independent 
condition.  It  is  difficult  to  distinguish  between  catarrh  and  inflamma- 
tion of  the  bronchi.  In  passive  congestion  of  the  lungs  and  bronchi, 
and  in  bronchial  asthma,  the  bronchial  disturbance  is  usually  at  first 
catarrhal,  and  becomes  inflammatory  only  after  an  infection  compli- 
cates the  process,  but  it  is  difficult  to  judge  when  the  one  ends  and  the 
other  begins,  and  it  therefore  seems  best  to  describe  the  two  condi- 
tions under  a  common  heading. 

Etiology. — There  are  three  groups  of  cases  depending  on  the  seat 
of  the  underlying  disease  in  the  circulatory  system,  the  lungs  or  the 
bronchi. 

Circulatory  System. — Passive  congestion  of  the  pulmonary  circuit  in 
consequence  of  cardiac  insufficiency  is  the  most  common  cause,  and  the 
resulting  bronchial  disturbance  is  often  spoken  of  as  a  "  stasis  catarrh." 
This  occurs  in  a  small  proportion  of  patients  in  the  later  stages  of  broken 


CHRONIC  BRONCHITIS  95 

compensation  from  valvular  disease,  or  chronic  adhesive  pericarditis 
and  myocardial  weakness  from  disease  of  the  coronary  arteries, 
arteriosclerosis  of  the  aorta  or  chronic  nephritis.  Syphilitic  aortitis 
is  not  uncommon  as  a  cause  of  the  cardiac  failure.  Aortic  aneurysm 
may  be  a  cause  as  the  result  of  congestion  of  the  pulmonary  circuit 
from  cardiac  insufficiency  or  give  rise  to  localized  forms  of  chronic- 
bronchitis  in  connection  with  bronchostenosis  from  compression  of 
the  bronchi.  Of  161  cases  with  symptoms  of  chronic  bronchitis  coming 
to  autopsy  at  the  Massachusetts  General  Hospital,  the  condition  was 
apparently  due  to  circulatory  disturbance  in  consequence  of  such 
causes  as  those  just  mentioned  singly  or  combined  in  103  (63  per  cent.). 
In  seven  of  nine  patients  who  gave  a  history  of  regularly  recurring 
winter  cough,  cardiac  insufficiency  in  consequence  of  arteriosclerosis 
of  the  aorta,  valvular  disease  or  chronic  nephritis  was  found  at  autopsy 
as  a  probable  underlying  cause.  An  aggravation  of  the  cardiac  failure 
during  the  stress  of  winter  weather  is  probably  responsible  for  the 
majority  of  such  cases.  In  others,  the  winter  cough  may  be  ascribed 
to  a  mild  and  persistent  infection  with  organisms  always  present  and 
ready  to  multiply  under  the  conditions  of  lowered  resistance. 

Pulmonary  Disease. — Of  diseases  of  the  lung,  infection  with  the 
tubercle  bacillus  occupies  first  place,  and  is  represented  in  this  series 
by  31  cases  (19  per  cent.),  of  which  22  were  chronic  ulcerative  tubercu- 
losis, and  the  remaining  nine  the  miliary  form  of  the  disease.  Con- 
cerning miliary  tuberculosis,  it  should  be  noted,  however,  that  bron- 
chitis is  an  unusual  feature,  and  that  a  large  majority  of  such  cases 
run  their  course  without  bronchial  manifestations.  As  in  the  bronchitis 
of  stasis,  so  here  also  the  growth  of  organisms  commonly  present  in 
the  respiratory  tract  is  probably  favored  by  the  abnormal  local  con- 
ditions, and  the  bronchitis  is  due  not  to  the  tubercle  bacillus  but  to 
secondary  invaders.  The  most  striking  example  of  such  secondary 
invasion  occurred  in  a  patient  with  an  intense  and  persistent  general 
bronchitis  and  the  constant  presence  of  pneumococci  in  the  sputum. 
Postmortem  examination  after  an  illness  of  eleven  weeks  showed  dis- 
seminated miliary  tubercles  in  the  lungs  and  other  organs.  Recurring 
winter  cough  may  be  observed  in  chronic  pulmonary  tuberculosis,  as 
in  one  of  this  series. 

Non-tuberculous  pulmonary  infection  is  responsible  for  a  large 
proportion  of  the  remaining  cases.  Measles,  whooping  cough,  and 
"grippe"  may  initiate  the  disturbance.  Chronic  infection  in  the  upper 
parts  of  the  tract  such  as  rhinitis,  pharyngitis  or  tonsillitis  may  be 
the  starting  point  of  the  disease.  The  inhalation  of  dust  as  a  carrier 
of  infectious  material  is  a  predisposing  cause.  Non-tuberculous 
pulmonary  infection  in  the  form  of  subacute  or  chronic  broncho- 
pneumonia, lobar  pneumonia  with  abscess  formation  and  abscess  and 
gangrene  was  found  at  autopsy  in  15  (9  per  cent.)  of  the  cases  in  this 
series.  Bronchiectasis  was  associated  in  4  cases.  Abscesses  too  small 
to  give  rise  to  physical  signs  may  be  demonstrated  at  autopsy  in  a 


96  DISEASES  OF  THE  BRONCHI 

small  proportion  of  the  bronchopneumonias,  and  such  defects  may 
remain  in  those  who  survive  as  permanent  pockets  for  the  develop- 
ment of  bacteria.  Elastic  tissue  with  an  alveolar  arrangement  may 
occasionally  be  found  in  the  sputum  without  evidence  of  losses  of 
pulmonary  substance  on  physical  examination  and  in  the  absence  of 
tubercle  bacilli,  and  it  is  probable  that  persistance  of  cough  and  signs 
of  localized  or  diffuse  bronchitis  are  usually  due  to  chronic  pulmonary 
infection.  Chronic  bronchitis  develops  in  the  tubes  leading  to  the 
infected  territory,  and  this  is  in  turn  followed  by  bronchiectasis. 

Malignant  disease  of  the  lung  or  mediastinal  glands  may  be  compli- 
cated by  chronic  bronchitis.  There  were  5  such  cases  in  the  present 
series.  Echinococcus  disease,  distomatosis,  pulmonary  embolism 
and  thrombosis,  syphilis,  actinomycosis  and  pneumonoconiosis  may  be 
similarly  complicated. 

Bronchial  Disease. — There  are  cases  in  which  attacks  of  bronchitis 
recur  during  a  period  of  many  years,  finally  terminate  in  more  or  less 
persistent  cough  and  expectoration,  and  at  autopsy  the  bronchi  are 
diffusely  involved  with  or  without  bronchiectasis.  Emphysema  is 
usually  present,  and  the  patients  die  from  intercurrent  pulmonary 
infection,  progressive  hypertrophy  and  dilatation  of  the  heart,  with 
increasing  passive  congestion,  or  pulmonary  embolism  and  thrombosis. 
The  absence  of  independent  circulatory  or  renal  disease  suggests  the 
dependence  of  the  cardiac  insufficiency  on  chronic  bronchitis  and 
emphysema.  The  clinical  records  of  such  cases  usually  indicate  that 
they  have  suffered  from  bronchial  asthma,  as  in  six  cases  (3.7  per  cent.) 
in  the  present  series. 

It  is  possible  that  a  chronic  diffuse  catarrh  may  remain  limited  to 
the  bronchi  and  exist  as  an  independent  condition  apart  from  passive 
congestion,  pulmonary  disease  or  bronchial  asthma,  but  it  is  difficult  to 
understand  how  an  infection  can  remain  strictly  limited  to  the  bronchi 
for  long  periods  without  extension  of  the  inflammation  to  the  peri- 
bronchial and  pulmonary  tissue.  Diffuse  purulent  bronchitis  and 
bronchiectasis  may  be  seen  in  connection  with  chronic  interstitial 
pneumonia  and  multiple  pulmonary  cavities  without  a  history  of 
asthma,  and  the  bronchial  manifestations  may  predominate  in  the 
clinical  picture,  but  it  is  difficult  to  differentiate  the  site  of  the  primary 
disturbance  in  such  cases  in  the  lung  or  the  bronchi. 

Many  cases  of  asthma  are  sooner  or  later  complicated  by  bacterial 
infection,  and  their  classification  in  this  or  the  preceding  group  may 
then  be  difficult  of  determination.  It  is  to  be  remembered  also  that 
bronchial  asthma  is  relatively  uncommon  in  comparison  with  other 
causes  of  chronic  bronchitis,  and  that  asthmatic  symptoms  are  fre- 
quent in  patients  with  passive  pulmonary  congestion  from  cardiac 
insufficiency. 

Chronic  bronchitis  is  observed  in  connection  with  bronchostenosis 
from  any  of  the  causes  mentioned  in  the  preceding  sections.  Syphilis 
of  the  trachea  and  bronchi  was  found  at  autopsy  in  one  patient  who 


CHRONIC  BRONCHITIS  97 

had  complained  of  recurring  winter  cough  and  died  of  hemorrhage 
from  rupture  of  a  syphilitic  cicatrix  of  one  of  the  primary  bronchi 
into  the  left  pulmonary  artery.  The  pressure  on  the  trachea  or  bronchi 
of  enlarged  tuberculous  mediastinal  and  bronchial  glands  may  give 
rise  to  irritative  cough  and  is  more  especially  a  cause  in  children. 

Disease  of  the  Nasopharynx  and  Tonsils. — In  children,  and  at  times 
in  adults,  enlargement  of  the  tonsils,  the  adenoids  and  other  lymphoid 
tissue  of  the  nasopharynx  is  associated  with  chronic  nasopharyngeal 
catarrh  and  mouth  breathing.  Secretion  which  accumulates  on  the 
posterior  pharyngeal  wall  is  hawked  up  or  expelled  by  cough.  Some 
irritation  of  the  larynx  and  hoarseness  may  also  be  present.  Infection 
in  the  tonsils  or  adenoids  may  be  the  starting  point  of  infections  of  the 
deeper  parts  of  the  tract. 

Other  Causes. — There  has  been  a  disposition  to  regard  many  cases 
of  chronic  bronchitis  as  due  to  a  constitutional  anomaly  and  to  include 
under  this  heading  those  examples  of  the  condition  in  which  the  cause 
is  vague  or  intangible.  The  study  of  the  161  cases  in  this  series,  how- 
ever, seems  to  indicate  that  while  for  long  periods  the  cause  may  be 
obscure  and  perhaps  undiscoverable  clinically,  yet  the  cases  can  be 
grouped  almost  without  exception  under  the  three  classes  already 
given  when  postmortem  examinations  are  made,  and  many  cases 
ascribed  to  indefinite  causes  probably  belong  in  one  of  the  groups 
cited  above.  Cases  due  to  cardiac  decompensation  have  probably 
most  often  given  rise  to  confusion  owing  to  the  difficulty  of  decid- 
ing clinically  whether  the  circulatory  disturbances  are  primary  or 
secondary. 

An  inherited  disposition  to  chronic  bronchitis  has  been  noted  by 
various  writers,  but  is  probably  of  little  moment  except  in  so  far  as  a 
tendency  to  the  development  of  arteriosclerosis  or  bronchial  asthma 
can  be  regarded  as  a  family  disease.  Gout  and  obesity  are  of  impor- 
tance as  factors  in  leading  to  disturbances  in  the  circulation  and  cardiac- 
weakness.  Alcohol  has  been  regarded  as  a  cause  and  its  excretion  by 
the  bronchi  suggested  in  explanation.  Among  the  Germans,  "  schnapps- 
catarrh"  is  a  recognized  form,  but  stasis  in  the  pulmonary  circuit 
is  a  more  probable  cause.  Contagion  is  of  importance  in  those  forms 
in  which  an  infection  can  be  transmitted  from  person  to  person. 
There  is  no  evidence  that  the  use  of  tobacco  is  capable  of  causing 
bronchitis.  The  alternation  of  attacks  of  eczema  and  bronchitis  has 
been  thought  to  indicate  a  relation  between  the  two,  but  is  so  uncom- 
mon as  to  suggest  nothing  more  than  coincidence.  The  supposition 
that  bronchitis  can  be  referred  to  disturbances  in  the  gastrointes- 
tinal tract  has  no  foundation  in  fact.  Such  terms  as  dentition-, 
stomach-,  liver-,  intestine-,  spleen-,  and  uterine-cough  and  arthritic- 
and  albuminuric-bronchitis  are  far  from  describing  any  actual 
condition. 

Age  and  Sex. — Age  is  of  some  importance  in  the  etiology,  but  very 
variable  in  the  individuals  making  up  the  different  groups.  Patients 
7 


98  DISEASES  OF   THE  BRONCHI 

with  arteriosclerosis  as  a  cause  are  usually  past  middle  life  and  often 
over  sixty,  while  those  with  valvular  disease  and  pulmonary  infection 
average  between  thirty  and  forty  when  they  first  come  under  observa- 
tion. Of  the  6  cases  with  bronchial  asthma,  two  were  forty,  two 
between  thirty-five  and  forty,  and  one  twenty-five  at  the  onset  of 
symptoms.  The  last  patient,  a  woman  of  sixty-five,  stated  that  she 
had  had  asthma  "all  her  life."  Males  in  general  far  exceed  females, 
the  proportion  being  3  :  1  in  this  series. 

Pathology. — The  changes  are  variable.  Swelling  and  redness  may 
be  seen  in  the  chronic  as  in  the  acute  form.  This  represents  what  may 
be  spoken  of  as  the  hypertrophic  variety,  in  which  the  mucous  mem- 
brane is  thickened  and  indurated  and  presents  a  villous,  shaggy,  or 
velvety  appearance  in  consequence  of  the  abundant  new  formation 
of  bloodvessels.  Proliferation  of  the  glands  may  also  take  place. 
Microscopic  examination  may  show  cellular  infiltration  of  all  parts 
of  the  bronchial  wall.  The  thickening  and  induration  may  extend  to 
the  peribronchial  and  neighboring  pulmonary  tissue.  In  the  atrophic 
form,  following  the  round-celled  infiltration  and  transformation  into 
connective  tissue,  the  glands,  muscle  fibers  and  even  the  cartilages 
atrophy  and  the  mucous  membrane  is  desquamated.  Ulceration  of 
the  mucous  follicles  may  be  observed.  The  bronchi  are  converted 
into  inelastic  tubes  and  are  often  dilated  in  consequence  of  the  stasis 
of  secretion  and  the  pressure  to  which  they  are  subjected  by  cough 
with  the  glottis  closed.  Emphysema  may  occur,  and  is  most  common 
when  asthma  is  the  underlying  cause  of  the  bronchial  changes.  Hyper- 
trophy and  dilatation  of  the  heart  may  be  a  consequence  of  the  increase 
of  pressure  in  the  pulmonary  circuit. 

Symptoms. — Cough,  expectoration  and  varying  degrees  of  dyspnea 
are  common  to  all  cases,  but  the  order  of  their  appearance,  their 
intensity  and  character  differ  in  the  different  groups. 

With  passive  congestion  as  a  cause,  dyspnea  is  usually  the  first 
symptom  and  cough  is  added  after  a  longer  or  shorter  interval.  In 
other  cases  cough  and  dyspnea  occur  together  at  the  onset.  In  rare 
instances,  cough  is  the  first  symptom  and  after  a  time  is  followed  by 
dyspnea.  This  unusual  sequence  is  illustrated  in  the  case  of  a  man  aged 
sixty-six  years  (Autopsy  462)  who  complained  of  cough,  scanty  expec- 
toration and  wheezing,  more  especially  at  night,  for  two  to  three  win- 
ters, but  without  dyspnea  until  about  nine  months  before  his  death. 
The  dyspnea  was  then  only  slight  and  did  not  prevent  continuance 
at  his  work  of  lifting  in  a  lumber  yard.  Edema  appeared  two  or  three 
weeks  before  his  death,  and  at  postmortem  examination  the  aorta 
and  great  branches  were  dilated,  tortuous,  and  markedly  sclerotic. 
The  heart  was  hypertrophied  and  dilated,  but  there  were  no  other 
significant  changes  than  a  marked  degree  of  chronic  passive  congestion 
in  the  lungs,  liver,  spleen  and  kidneys,  and  hydrothorax  and  anasarca. 
In  this  group,  the  cough  is  usually  little  troublesome  at  first,  may  be 
started  by  some  unusual  exertion  and  persist  for  a  time  thereafter,  or 


CHRONIC  BRONCHITIS  99 

occur  on  lying  down  or  in  the  morning  on  rising.  It  may  be  accom- 
panied or  replaced  by  wheezing.  Once  started,  cough  is  usually  per- 
sistent throughout  the  course  of  the  disease,  but  may  consist  of  a  suc- 
cession of  attacks,  each  tending  to  last  longer  than  those  which  have 
preceded.  Such  attacks  are  more  likely  to  occur  in  the  winter  months, 
with  partial  or  complete  freedom  during  the  summer.  They  usually 
differ  from  ordinary  attacks  of  bronchitis  in  the  absence  of  initial 
symptoms  referred  to  the  upper  parts  of  the  tract,  the  scanty  expec- 
toration and  afebrile  course.  The  cough  may  long  precede  death. 
Among  106  cases  in  this  series,  32  had  lasted  one  year  or  longer,  and 
of  these,  14,  five  years  or  more,  and  2,  twenty  to  thirty  years.  Expec- 
toration is  at  first  absent,  or  scanty,  and  usually  consists  of  only  small 
amounts  of  frothy,  white,  thin,  watery  or  mucoid  material,  with  or 
without  blood  in  streaks,  masses  or  homogeneous  admixture.  Copious 
amounts  of  sputum  may  be  seen  with  acute  pulmonary  edema.  If  an 
infection  is  present,  the  sputum  is  mucopurulent  or  purulent. 

The  dyspnea  is  at  first  chiefly  noted  on  exertion,  finally  becomes 
persistent,  and  is  likely  to  be  worse  at  night.  Attacks  resembling 
bronchial  asthma  may  be  observed.  Orthopnea  and  edema  occur 
late  in  the  course  of  the  disease.  On  examination  the  lungs  may  be 
negative,  or  non-consonating  fine,  medium  or  coarse  rales  may  be 
heard.  They  may  be  confined  to  the  bases  behind  or  at  times  are  more 
widely  distributed  over  the  chest,  but  most  numerous  at  the  dependent 
parts.  In  some  cases  sibilant  and  sonorous  rales  are  heard  throughout 
both  lungs.  Emphysema  is  a  complication  in  rare  instances.  The 
pulmonary  symptoms  and  signs  do  not  differ  in  any  essential  particular 
according  to  the  cause  of  the  cardiac  failure,  but  a  clinical  distinction 
can  usually  be  made  between  the  different  causes  from  other  features 
of  the  case.  A  further  discussion  of  passive  congestion  will  be  found 
in  the  section  on  that  subject. 

When  bronchitis  occurs  as  a  complication  of  tuberculous  or  non- 
tuberculous  pulmonary  infection,  it  is  usually  characterized  by  cough 
as  an  early  symptom  and  the  expectoration  of  mucopurulent  or  puru- 
lent sputum.  In  both  groups  the  chronic  cough  may  be  initiated  by 
some  well-defined  acute  infection,  but  in  many  instances  the  onset  is 
insidious.  Cough  and  expectoration  are  the  most  prominent  features 
of  the  illness.  Dyspnea  becomes  manifest  after  some  time  has  elapsed 
and  in  consequence  of  the  extension  of  the  lesions  or  the  development 
of  emphysema.  Climate  and  season  influence  such  cases,  an  improve- 
ment being  almost  constantly  observed  in  a  warm  equable  temperature 
with  freedom  from  dust,  and  during  the  summer  months.  These 
causes  are  for  the  most  part  concerned  in  the  production  at  first  of 
localized  forms  of  bronchitis,  but  as  the  disease  progresses,  broncho- 
pulmonary infection  may  spread  from  the  original  site  of  infection  to 
the  greater  part  or  the  whole  of  one  or  both  lungs.  General  emphysema 
and  symptoms  of  cardiac  weakness  are  uncommon  unless  the  pul- 
monary infection  is  a  complication  of  asthma.     In  non-tuberculous 


101)  DISEASES  OF  THE  BRONCHI 

cases  the  course  is  afebrile  unless  complicated  by  intercurrent  broncho- 
pneumonia or  other  septic  infection. 

The  chronic  bronchitis  of  asthma  is  characterized  by  the  occurrence 
of  sudden  attacks  of  dyspnea,  affecting  both  phases  of  respiration,  but 
especially  expiration.  Emphysema  is  almost  constantly  observed. 
Sibilant  and  sonorous  rales  throughout  both  lungs  are  usually  present. 
An  eosinophilia  in  the  sputum  and  the  circulating  blood  may  be  deter- 
mined. Curschmann  spirals  and  Charcot-Leyden  crystals  may  also 
be  found.  The  disease  usually  begins  under  forty  and  may  last  for 
many  years.  By  the  time  persistent  cough  and  expectoration  have 
developed,  the  sputum  is  likely  to  have  changed  from  its  tenacious 
mucoid  character  to  mucopurulent  or  purulent.  The  condition  is 
further  discussed  in  the  section  on  Asthma. 

Clinical  Varieties. — If  cases  are  grouped  according  to  the  character 
of  the  expectoration,  the  following  classes  may  be  observed. 

1.  Dry  Catarrh. — Catarrhe  sec  is  a  term  applied  by  Laennec1  to  an 
inflammation  of  the  bronchi  with  little  or  no  expectoration.  The 
expectoration  when  present  consists  of  small,  tenacious,  grayish,  semi- 
transparent  masses  not  unlike  boiled  sago,  and  was  termed  crachats 
-perl is  by  Laennec.  Microscopic  examination  shows  numerous  large 
round,  mononuclear  cells  resembling  alveolar  epithelium  and  often 
containing  pigment  granules.  Ciliated  epithelium,  polymorphonu- 
clear leukocytes,  eosinophiles  and  bacteria  are  usually  present  only 
in  small  numbers.  Dyspnea  is  a  prominent  symptom,  at  first  only 
on  exertion,  later  while  at  rest,  and  at  times  to  such  a  degree  as  to 
resemble  that  in  asthma.  Cough  and  expectoration  begin  toward  the 
termination  of  the  attack,  and  with  their  appearance  the  dyspnea 
diminishes.  The  cough  may  be  dry,  or  for  the  most  part  without  ex- 
pectoration and  recurs  only  once  in  the  twenty-four  hours  or  only  every 
two  or  three  days.  It  may  cease  during  the  summer.  On  examination 
an  occasional  sibilant  or  non-consonating  moist  rale  may  be  heard. 
In  places  the  respiratory  murmur  may  be  diminished  or  absent  for 
a  time,  and  then  again  become  normal,  probably  in  consequence  of 
varying  degrees  of  engorgement  of  the  bronchial  mucous  membrane 
over  the  affected  regions  and  the  occlusion  of  the  passages  by  tenacious 
secretion  or  its  expulsion  by  cough. 

Pathologically,  according  to  Laennec,  the  mucous  membrane  of  the 
bronchi  is  swollen  and  of  a  red  or  violet  color.  The  swelling  is  most 
marked  in  the  small  branches  which  may  at  times  be  entirely  obstructed. 
The  obstruction  may  be  due  to  swelling  of  the  mucous  membrane  or  to 
the  accumulation  of  viscid  secretion  such  as  that  found  in  the  sputum. 
Extensive  or  universal  involvement  of  the  bronchi  is  followed  by  the 
development  of  emphysema. 

The  cause  of  the  catarrhe  sec  of  Laennec  is  not  clear.  The  cases 
conform  in  their  clinical  aspect  to  those  in  which  passive  congestion 

1  Traite  dc  l'auscultation  med.,  T.  i,  p.  203, 


CHRONIC  BRONCHITIS  101 

is  responsible  for  the  symptoms.  Slight  degrees  of  congestion  in  the 
pulmonary  circuit  may  predispose  to  catarrhal  inflammation  and  an 
increased  secretion  from  the  bronchial  mucosa.  The  cardiac  weakness 
is  insufficient  in  degree  to  give  rise  to  outspoken  pulmonary  edema  or 
the  expectoration  of  serous  fluid.  Bronchial  asthma  may  be  concerned 
in  some  cases  and  is  more  likely  to  be  a  cause  in  those  with  emphysema. 

2.  Eosinophile  Bronchitis. — Under  this  title,  Teichmuller1  has 
described  a  form  of  chronic  bronchitis  in  which  there  is  a  greater 
number  of  eosinophiles  than  in  ordinary  bronchitis.  There  is  moderate 
dyspnea  and  in  the  less  favorable,  relapsing  cases  emphysema  of  the 
pulmonary  margins.  Dry  sonorous  and  sibilant  rales  and  prolonged 
expiration  are  heard  on  auscultation.  The  sputum  is  transparent  and 
mucoid.  Eosinophiles  are  present  in  abundance  in  the  mucus,  and  here 
and  there  may  be  the  only  cells  in  the  cellular  parts  of  the  sputum. 
Desquamated  bronchial  epithelium  and  red-blood  cells  are  uncommon. 
Charcot-Leyden  crystals  may  be  present  and  imperfectly  developed 
forms  of  Curschmann's  spirals  with  central  threads  are  at  times  found. 
Miiller2  found  an  eosinophilia  of  10  to  13  per  cent,  in  the  blood  of 
one  case. 

The  disturbance  is  probably  a  rudimentary  form  of  bronchial  asthma. 
Varying  and  usually  only  small  numbers  of  eosinophiles  are  found  in 
the  sputum  in  acute  bronchitis  and  in  chronic  bronchitis  secondary 
to  passive  congestion  and  tuberculous  and  non-tuberculous  pulmonary 
infections.  For  the  demonstration  of  eosinophiles  in  sputum,  Teich- 
muller spreads  the  sputum  on  a  glass  slide,  allows  it  to  dry  in  the  air 
and  fixes  it  over  the  flame.  While  still  warm  the  slide  is  immersed 
in  0.5  per  cent,  alcoholic  eosin  solution  for  five  minutes  or  longer. 
The  preparation  is  then  washed  in  water  and  counterstained  by  the 
application  for  two  minutes  of  a  concentrated  aqueous  solution  of 
methylene  blue.  Only  the  eosinophiles  retain  the  eosin  and  may  be 
readily  recognized  even  under  the  low  power  of  the  microscope. 

3.  Mucopurulent  and  Purulent  Bronchitis. — The  sputum  may  be 
largely  mucoid  with  admixture  of  pus  in  small  streaks  or  points,  or 
consist  of  larger  purulent  balls,  each  surrounded  and  prevented  from 
confluence  by  a  layer  of  mucus.  The  amount  is  variable.  In  long- 
standing cases  in  which  the  bronchitis  is  diffuse  and  associated  with 
bronchiectasis,  the  daily  amount  of  purulent  sputum  may  reach  a  pint 
or  more.  In  cases  in  which  the  bronchial  mucous  glands  are  atrophied 
the  sputum  may  consist  of  homogeneous  pus  with  little  mucus.  Dis- 
crete purulent  masses  surrounded  by  mucus  are  also  seen  with  ulcera- 
tive tuberculosis,  pulmonary  abscess  and  empyema  or  subdiaphrag- 
matic abscess  perforating  the  lung  when  the  purulent  material  is 
slowly  expectorated.  If  large  quantities  are  rapidly  evacuated  from 
a  cavity  the  pus  is  homogeneous  and  little  mixed  with  mucus. 

1  Deut.  Arch.  f.  klin.  Med.,  1898,  vol.  lx,  and  ibid.,  1899,  lxiii,  444. 

2  Deut.  Klinik,  1903-07,  p.  278. 


102  DISEASES  OF  THE  BRONCHI 

Bacteriologic  examination  usually  shows  a  mixed  infection  with 
two  or  more  organisms,  among  them  the  influenza  bacillus,  Micro- 
coccus catarrhalis,  the  pyogenic  cocci,  pneumococci,  Bacillus  mucosus 
capsulatus,  and  the  Streptococcus  capsulatus.  Comparatively  pure 
infections  with  one  organism  may  he  demonstrated  and  the  influenza 
bacillus  is  apparently  concerned  in  the  largest  number,  with  other 
organisms  in  a  smaller  proportion  of  the  chronic  cases.  Repeated 
examination  over  long  periods  usually  shows  that  one  group  of  organisms 
does  not  long  remain  unmixed  in  the  sputum. 

The  purulent  forms  of  bronchitis  are  not  independent  affections. 
In  many  cases  the  clinical  picture  may  be  predominantly  bronchial 
and  there  may  be  no  evidence  of  pulmonary  involvement  on  examina- 
tion. Invasion  of  the  pulmonary  tissue  may  safely  be  assumed  in 
chronic  cases,  however,  from  the  experience  at  the  autopsy  table. 
With  the  chronic  bronchitis,  bronchiectasis,  peribronchitis,  pulmonary 
abscesses,  and  chronic  interstitial  pneumonia  are  to  be  expected. 

4.  Putrid  Bronchitis. — Fetid  expectoration  is  occasionally  observed 
in  bronchitis  in  connection  with  bronchiectasis,  abscess,  gangrene, 
ulcerative  tuberculosis,  chronic  indurative  pneumonia,  and  empyema 
or  subphrenic  abscess  perforating  the  lung.  It  is  doubtful  if  it  exists 
as  a  chronic  condition  other  than  in  connection  with  changes  in  the 
lung.  The  cause  of  the  putrefaction  is  not  clear.  The  sputum  is 
abundant  and  foul,  of  a  dirty  green  or  yellowish  color,  and  on  standing 
tends  to  separate  into  an  upper  greenish  yellow,  opaque  fluid  capped 
with  frothy  mucus,  a  middle  zone  of  more  transparent  serous  fluid 
and  at  the  bottom  a  sediment  of  thick  pus  in  which  at  times  may  be 
found  dirty  yellow  or  white  mushy,  soft,  foul-smelling  masses  varying 
in  size  from  that  of  a  millet  seed  to  a  bean,  the  so-called  Dittrich's 
plugs.  Microscopic  examination  of  these  masses  shows  numerous 
bacteria,  leptothrix  threads,  fatty  acid  crystals,  occasional  pus  cells, 
and  detritus.  Symptoms  of  sepsis  are  usually  present  and  extension 
of  existing  bronchopulmonary  suppuration  is  likely  to  take  place  into 
previously  uninvolved  regions.  Acute  cases  may  recover,  but  in  the 
chronic  cases  the  outlook  is  grave. 

5.  The  Serous  Form  of  Catarrh. — (Bronchorrhea  serosa. — Catarrhe 
pituiteitx  of  Laennec.) — In  this  uncommon  form  a  profuse  liquid, 
watery,  clear  or  cloudy  fluid,  with  a  variable  amount  of  mucus  is 
expectorated.  Miiller1  finds  the  specific  gravity  low  (1004),  albumin 
present  only  in  traces,  and  on  microscopic  examination  only  few 
cells,  among  which  eosinophiles  predominate.  Isolated  Curschmann 
spirals  and  Charcot-Leyden  crystals  may  also  be  found.  Fluids  of 
this  character  are  consistent  with  increased  bronchial  secretion  and 
may  be  found  with  asthma  (asthma  humidum).  Miiller  observed 
the  expectoration  of  as  much  as  a  liter  a  day  of  thin,  frothy  sputum, 
with  a  specific  gravity  of  1003  and  almost  free  from  albumin  in  a 

1  Deut.  Klinik,  1903-07,  iv,  279. 


CHRONIC  BRONCHITIS  103 

patient  with  myasthenia  gravis  pseudoparalytica.  Isolated  Cursch- 
mann  spirals,  but  no  increase  in  eosinophiles  and  no  crystals  won; 
found.  Large  amounts  of  thin,  foamy  sputum  were  also  expectorated 
by  a  patient  with  severe  acute  polyneuritis  of  unknown  origin.  In 
this  case  a  rapid  pulse  suggested  involvement  of  the  vagus  in  the 
neuritic  process.  The  patient  recovered  and  with  the  fall  in  the  pulse 
rate  the  abundant  sputum  stopped.  Thin,  fluid  expectoration  may 
also  be  seen  as  a  result  of  pulmonary  edema  from  passive  congestion 
or  following  thoracentesis  (albuminous  expectoration).  A  larger 
percentage  of  albumin  and  higher  specific  gravity  will  serve  to  differ- 
entiate such  forms  from  the  preceding.  Wanner1  estimates  the  amount 
of  albumin  after  removal  of  mucin  by  the  addition  of  acetic  acid. 
To  a  measured  quantity  of  sputum  3  per  cent,  acetic  acid  is  added. 
The  mixture  is  energetically  shaken,  and  the  precipitated  mucus  fil- 
tered out.  The  albumin  is  estimated  directly  in  the  acid  filtrate  by 
means  of  potassium  ferrocyanide  solution  or  coagulated  by  heat  after 
neutralization  with  sodium  carbonate  or  sodium  hydrate. 

Complications. — Emphysema  is  one  of  the  most  frequent  complica- 
tions. It  may  be  seen  in  all  forms  of  chronic  bronchitis,  but  is  most 
frequently  observed  with  asthma.  Peribronchitis,  bronchiectasis,  and 
acute  and  chronic  pulmonary  infection  are  common.  Increased  resist- 
ance in  the  pulmonary  circuit  in  consequence  of  emphysema  may 
induce  cardiac  hypertrophy  and  dilatation.  Clubbing  of  the  fingers 
and  toes  may  be  noted.  It  is  more  common  in  connection  with  bron- 
chiectasis than  with  other  forms  of  bronchitis  and  is  more  fully  con- 
sidered in  that  section.  Metastatic  cerebral  abscess  may  complicate 
purulent  bronchitis.  Amyloid  degeneration  may  be  a  consequence 
of  long-continued  bronchopulmonary  suppuration. 

Diagnosis. — Persistent  cough,  expectoration  and  rales  establish  the 
diagnosis  of  chronic  bronchitis,  but  the  diagnosis  should  never  be 
allowed  to  rest  here.  Chronic  bronchitis  is  almost  invariably  only  a 
symptom,  the  cause  of  which  must  be  determined  before  the  problem 
can  be  regarded  as  solved. 

Evidence  of  bilateral  or  diffuse  chronic  bronchitis  occurring  in  a 
person  past  middle  life  and  with  winter  or  persistent  cough  and  scanty 
expectoration  should  be  suspected  of  cardiac  origin.  A  history  of 
dyspnea  preceding  the  onset  of  cough,  the  signs  of  cardiac  involvement 
from  valvular,  myocardial  or  pericardial  disease,  or  the  establishment 
of  arteriosclerosis  of  the  aorta,  aneurysm  or  chronic  nephritis  are  of 
importance  in  fixing  the  blame  on  the  circulatory  system.  Attacks 
of  dyspnea,  cyanosis  and  cough  with  scanty  sputum  or  wheezing 
beginning  in  persons  past  middle  life  are  more  often  due  to  cardiac 
than  to  bronchial  asthma. 

Bronchitis  due  to  tuberculous  or  non-tuberculous  pulmonary  infec- 
tion may  be  distinguished  by  the  occurrence  of  cough  and  mucopuru- 

1  Beitrage  z.  Chemie  d.  Sputums,  Deut.  Arch.  f.  klin.  Med.,  1902-03,  lxxv,  347. 


104  DISEASES  OF   THE  BRONCHI 

lent  or  purulent  expectoration  as  an  early  and  prominent  symptom, 
with  dyspnea  as  a  later  manifestation,  other  features  of  the  history, 
and  the  signs  of  pulmonary  involvement.  Even  without  other  evi- 
dence on  physical  examination  of  invasion  of  the  lung,  the  persistence 
of  rales  at  one  place  may  he  taken  as  an  indication  of  involvement 
of  the  lung  tissue  rather  than  of  the  bronchi  alone.  Moist  rales  of  a 
consonating  character  are  also  suggestive.  The  signs  of  cavity  may 
be  present.  Examination  of  the  sputum  may  show  tubercle  bacilli, 
actinomyces  or  elastic  tissue  with  an  alveolar  arrangement.  Radio- 
seopic  examination  will  assist  in  the  interpretation.  Tuberculosis 
should  be  rigidly  exeluded  before  a  diagnosis  of  a  simpler  infection  is 
made.  In  doubtful  cases,  tuberculin  may  be  given  after  other  means 
of  investigation  have  been  exhausted. 

Bronchial  asthma  may  be  distinguished  by  a  history  of  typical  attacks 
beginning  in  youth  or  early  life  with  intervals  of  comparative  freedom 
or  complete  absence  of  pulmonary  symptoms  between  the  paroxysms. 
Examination  of  the  sputum  and  the  blood  may  assist  in  the  diagnosis. 
Persistent  cough,  mucopurulent  or  purulent  sputum,  emphysema 
and  dyspnea  with  signs  of  failing  cardiac  compensation  may  develop 
after  a  time,  and  it  may  then  be  difficult  to  differentiate  between 
passive  congestion  with  cardiac  asthma  and  bronchial  asthma  with 
secondary  cardiac  insufficiency. 

Diffuse  rales  with  a  sibilant  and  sonorous  quality  are  common  to 
both  conditions,  but  more  frequent  with  bronchial  asthma.  Emphy- 
sema of  an  extreme  grade  is  seldon  observed  in  passive  congestion. 
It  is  common  in  bronchial  asthma.  Hypertrophy  and  dilatation  of  the 
heart  from  increased  resistance  in  the  pulmonary  circuit  is  frequently 
associated  with  blowing  systolic  murmurs  at  the  apex  from  relative 
mitral  insufficiency,  but  hypertrophy  and  dilatation  from  other  causes 
may  be  indicated  by  the  presence  of  other  valvular  lesions.  Primary 
myocardial  disease  may  be  suggested  by  a  history  of  angina.  Chronic 
adhesive  pericarditis  should  be  excluded.  A  rough  systolic  murmur 
of  maximum  intensity  in  the  second  right  interspace  and  transmitted 
to  the  neck  may  indicate  arteriosclerosis  of  the  aorta.  A  positive 
Wassermann  test  may  confirm  the  suspicion  of  syphilitic  aortitis. 
Radioscopic  examination  will  assist  in  the  diagnosis  of  aneurysm.  A 
blood-pressure  of  200  mm.  Hg.  or  over  should  suggest  chronic  nephritis. 

Foreign  bodies  are  to  be  considered  in  the  localized  forms  of  apparent 
simple  chronic  bronchitis,  more  especially  in  children.  X-ray  examina- 
tion will  be  of  assistance  in  their  exclusion.  Syphilis  of  the  trachea 
and  bronchi  may  be  suggested  by  a  history  of  the  disease,  late  syphilitic 
lesions  elsewdiere,  and  a  positive  Wassermann  test.  Bronchoscopic 
examination  may  be  of  assistance  in  these  as  well  as  in  other  con- 
ditions. 

Prognosis. — This  is  that  of  the  underlying  condition  and  is  always 
serious.  In  the  cases  due  to  passive  congestion,  the  outlook  depends 
on  the  cause  of  the  cardiac  weakness  and  the  possibility  of  adequate 


CHRONIC  BRONCHITIS  105 

measures  for  its  relief.  It  can  be  estimated  only  after  thorough  con- 
sideration of  the  individual  case,  and  even  then  only  in  general  terms. 
In  rare  instances  the  bronchitis  is  one  of  the  earliest  manifestations 
and  may  precede  death,  as  in  one  of  the  hospital  series,  for  as  long 
as  thirty  years.  Much  may  depend  on  the  period  at  which  the  diag- 
nosis is  made.  The  prognosis  of  the  cases  due  to  pulmonary  infection 
and  bronchial  disease  will  be  found  in  the  separate  sections  dealing 
with  the  conditions  to  which  the  bronchitis  is  secondary.  In  some 
instances  the  bronchopulmonary  infection  may  last  for  years  and  tens 
of  years  with  little  apparent  disturbance  of  the  general  health.  In 
one  of  the  present  series  (Autopsy  1037)  there  was  a  history  of  cough 
and  purulent  expectoration  for  forty-four  years. 

Treatment. — As  chronic  bronchitis  is  usually  a  symptom  and  not 
an  independent  disorder,  the  treatment  should  be  directed  against  the 
cause.  It  is  important  to  remember  that  a  cough  which  is  due  to 
excessive  secretion  is  necessary  for  the  expectoration  of  accumulated 
material,  and  that  measures  directed  toward  the  suppression  of  the 
cough  without  removing  its  cause  do  not  strike  at  the  root  of  the 
trouble,  and  if  successful,  would  be  likely  to  aggravate  the  underlying 
disturbance.  With  the  exception  of  syphilis,  none  of  the  conditions 
causing  chronic  bronchitis  are  susceptible  of  specific  medication  and 
cure.  When  an  arrest  of  the  process  is  secured,  it  is  usually  due  to  the 
recuperative  powers  of  the  patient,  assisted,  it  may  be,  by  helpful 
suggestions  as  to  a  more  healthy  mode  of  life.  Reliance  should  be 
placed  chiefly  on  the  avoidance  of  deleterious  influences  and  efforts 
to  increase  individual  resistance.  Vaccines,  sera  and  drugs  have 
thus  far  proved  valueless  as  curative  measures.  Some  alleviation  of 
symptoms  occasionally  follows  the  use  of  certain  drugs. 

In  cases  in  which  the  chronic  bronchitis  is  dependent  on  failure 
of  the  circulation,  the  largest  single  group,  treatment  should  be  directed 
against  the  cause  of  the  cardiac  failure  and  the  compensation  restored 
and  maintained.  Although  already  existing  lesions  may  be  irremediable, 
yet  an  effort  should  be  made  to  stop  their  further  progress  by  appro- 
priate means.  Treatment  against  syphilis  should  be  instituted  in 
patients  with  this  disease.  Etiologic  factors  for  other  forms  of  arterio- 
sclerosis should  be  sought  and  removed.  Further  infection  of  a  chronic 
valvular  endocarditis  should,  if  possible,  be  prevented  by  removal  of 
a  primary  focus  of  infection  in  any  part  of  the  body.  The  tonsils 
should  be  especially  considered  in  this  connection.  Chronic  nephritis, 
if  present,  should  be  treated.  For  the  restoration  and  maintenance  of 
cardiac  compensation  much  may  be  done,  and  chief  reliance  may  well 
be  placed  on  measures  which  spare  the  already  overtaxed  heart. 
Rest  is  of  prime  importance,  the  amount  recommended  being  dependent 
on  the  degree  of  decompensation.  Directions  as  to  the  diet,  the  amount 
of  liquid  intake,  the  quantity  of  salt  ingested,  and  the  regulation  of  the 
bowels  should  be  given.  In  the  more  severe  types  of  cardiac  failure 
digitalis  should  be  used.     If  acute  cardiac  failure  with  overfilling  of 


106  DISEASES  OF   THE  BRONCHI 

the  right  side  <>f  the  heart  supervenes,  venesection  may  be  of  great 
benefit. 

The  recurring  winter  cough  of  elderly  persons  is  usually  a  symptom 
of  cardiac  strain  during  the  stress  of  winter  weather.  An  increased 
liability  to  bronchial  infection  obtains  in  some  patients  with  mild 
degrees  of  broken  compensation.  For  such  patients,  in  addition  to  the 
means  already  indicated,  such  preventive  measures  as  are  mentioned 
under  Prophylaxis  in  the  chapter  on  Acute  Bronchitis  are  applicable. 
If  the  financial  status  permits,  the  winter  may  well  be  passed  in  a 
southern  latitude.  An  alleviation  of  or  freedom  from  symptoms  may 
be  found  in  southern  California,  Florida,  Cuba,  Jamaica  or  Bermuda, 
in  the  United  States,  and  the  Mediterranean  coast,  Egypt,  Sicily, 
Madeira,  or  the  Canary  Islands,  in  Europe. 

The  bronchitis  secondary  to  pulmonary  infection  with  the  tubercle 
bacillus,  or  other  organisms,  should  be  treated  as  indicated  in  other 
sections.  Rest  in  bed  while  there  is  fever,  improvement  of  the  nutri- 
tion by  abundant  food,  and  fresh  air  by  night  as  well  as  by  day  are 
important  in  the  non-tuberculous  as  in  the  tuberculous  cases.  The 
treatment  of  bronchial  asthma,  syphilis  of  the  bronchi,  foreign  bodies, 
and  other  forms  of  bronchitis  is  considered  elsewhere. 

Measures  applicable  to  all  forms  of  bronchitis  may  be  considered 
under  the  following  headings: 

Hygienic  Treatment. — During  exacerbations  of  the  chronic  form,  as 
well  as  during  acute  attacks  of  bronchitis,  it  is  well  for  the  patient  to 
remain  at  home,  or  if  greater  freedom  is  permitted,  to  allow  him  out 
in  the  open  only  when  the  air  is  still  and  free  from  dust.  Mouth 
breathing  should  be  avoided,  and  the  clothing  should  be  sufficiently 
warm  to  prevent  chilling  of  the  body.  Woolen  undergarments  are  to 
be  preferred  both  for  summer  and  winter.  Hot,  dusty  or  smoky 
rooms  are  to  be  avoided. 

Hydrotherapy  may  increase  the  patient's  resistance  and  prevent 
exacerbations  or  reinfections.  In  patients  unaccustomed  to  cool 
baths,  water  at  a  temperature  of  75  to  80  degrees  may  first  be  used, 
and  the  body  bathed  in  sections,  beginning  with  the  arms,  then  the 
chest,  back,  and  finally  the  legs,  each  part  being  moistened  with  a 
large  sponge,  then  dried  and  rubbed  with  a  harsh  bath  towel  before 
proceeding  to  the  next.  The  temperature  of  the  water  may  be  grad- 
ually lowered,  and  the  amount  of  surface  bathed  at  one  time  increased, 
until  finally  the  patient  takes  a  full  bath  at  the  temperature  of  the 
tap  water  each  morning.  A  good  reaction  should  be  secured  after 
the  bath. 

Posture. — Elevation  of  the  foot  of  the  bed  and  the  assumption  of  an 
inclined  position  of  the  body  several  times  during  the  day,  as  described 
under  the  treatment  of  bronchiectasis,  may  assist  in  more  thoroughly 
evacuating  the  bronci  of  accumulated  secretion. 

Local  Treatment. — The  injection  of  medicated  fluids  into  the  trachea 
and  bronchi  is  now  seldom  used.     A  solution  of  5  to  10  per  cent. 


CHRONIC   BRONCHITIS  107 

menthol  in  olive  oil  is  sometimes  injected  by  means  of  a  suitable  syringe. 
The  larynx  is  anesthetized  with  4  per  cent,  cocain  and  the  end  of  the 
cannula  passed  through  the  glottis  under  the  direction  of  the  laryngo- 
scope. Iodoform  gr.  \  (0.032  gm.)  or  morphia  gr.  \  (0.008  gm.)  to 
drams  2  (8  c.c.)  of  olive  oil  may  be  substituted.  A  1  to  2  per  cent, 
solution  of  tannic  acid  is  occasionally  used.  Inhalation  of  the  vapor  of 
hot  water  or  hot  physiologic  salt  solution  may  be  helpful.  Creosote 
minims  5  to  20  (0.3  to  1.25  c.c),  eucalyptol  minims  5  to  20  (0.3  to  1.25 
c.c),  menthol  gr.  2  to  5  (0.130  to  0.325  gm.),  or  compound  tincture  of 
benzoin  dram  1  (4  c.c.)  may  be  added  to  a  pint  of  boiling  water  and  the 
vapor  inhaled.  A  solution  of  2  to  3  per  cent,  sodium  carbonate  may 
be  substituted.    A  spray  of  ipecacuanha  wine  is  sometimes  useful. 

Internal  Medication. — This  is  unsatisfactory,  but  a  host  of  drugs 
are  proposed.  Among  them,  iodid  of  potash,  in  small  doses  of  gr. 
2  to  3  (0.130  to  0.195  gm.),  gradually  increasing  to  gr.  10  to  15  (0.650 
to  0.975  gm.)  three  times  a  day  is  most  commonly  used.  Ammonium 
chloride  gr.  10  (0.650  gm.)  three  times  a  day  is  frequently  employed. 
Bicarbonate  of  sodium  gr.  15  (0.975  gm.),  chloride  of  sodium  gr.  5 
(0.325  gm.)  and  spirits  of  chloroform  minim  5  (0.3  c.c)  in  anise  water 
and  added  to  an  equal  quantity  of  warm  water  is  a  common  prescrip- 
tion. Terebene  minim  10  (0.6  c.c.)  and  terpene  hydrate  gr.  2  to  5 
(0.130  to  0.325  gm.)  may  be  tried.  When  cough  is  due  to  irritability 
of  the  mucous  membranes  and  is  unaccompanied  by  expectoration, 
heroin  gr.  TV  (0.005  gm.)  or  morphin  may  be  used.  Fetor,  if  present, 
may  be  lessened  by  the  administration  of  myrtol  gr.  2  to  5  (0.130  to 
0.325  gm.)  in  gelatin  capsules  three  or  four  times  a  day. 


CHAPTE  R   VI. 
BRONCHIECTASIS. 

Dilatatton  of  the  bronchi  is  only  in  rare  instances  an  independent 
affection,  but  usually  arises  as  a  complication  of  different  diseases  of 
the  bronchi,  lungs  and  pleura,  singly  or  combined.  At  times,  the 
features  of  bronchiectasis  predominate  in  the  clinical  picture,  thus 
justifying  its  separate  consideration.  The  condition  is  often  masked 
by  the  diseases  to  which  it  is  secondary,  and  it  is  thus  more  often  first 
discovered  at  autopsy  than  during  life.  We  owe  the  first  description 
of  bronchiectasis  to  Laennec,1  whose  attention  was  called  to  the  disease 
by  Cayol. 

Incidence. — Bronchiectasis  is  uncommon.  Laennec  saw  only  4 
cases,  2  of  which  were  Cayol's.  Its  incidence  among  clinical  cases 
varies  somewhat  with  the  character  of  the  material,  and  is  doubtless 
underestimated  from  the  difficulty  of  its  recognition.  Andral  described 
only  5  cases.  Barth2  collected  only  18  cases  during  fourteen  years  in 
the  general  hospitals  for  adults  in  Paris ,  25  cases  in  six  years  from  the 
hospital  for  old  women  in  the  Salpetriere.  Lebert3  observed  36  cases 
(20  men,  16  women.)  between  1860  and  1868  inclusive,  among  22,427 
patients  in  the  clinic  and  polyclinic  at  Breslau,  an  incidence  of  0.16 
per  cent.  Among  48,659  clinical  cases  at  the  Massachusetts  General 
Hospital,  the  disease  was  noted  in  only  38  (0.078  per  cent.).  Autopsy 
statistics  show  a  considerably  higher  proportion.  Willigk4  found  201 
cases  (4.4  per  cent.)  among  4546  autopsies  in  Prague  during  five  years. 
Biermer5  had  8  cases  (2  per  cent.)  of  essential  bronchiectasis  in  about 
400  postmortems  in  four  years  at  Berne.  King6  found  72  cases  (2.2 
per  cent.)  among  3227  postmortems  on  patients  with  thoracic  disease. 
(Brompton  Hospital  for  Diseases  of  the  Chest.)  At  the  Massachusetts 
General  Hospital,  to  which  patients  with  chronic  disease  are  very 
rarely  admitted,  only  7  cases  (0.3  per  cent.)  are  recorded  among  2200 
autopsies.  The  figures  are  somewhat  higher,  but  still  below  the  foreign 
statistics,  at  the  Boston  City  Hospital,7  where  38  cases  (1.19  per  cent.) 
were  found  among  3183  autopsies. 

Etiology. — No  age  is  exempt.  There  is  no  striking  predominance 
at  any  age.    The  disease  may  be  congenital.    It  is  relatively  uncommon 

1  Traite  de  l'auscultation  mediate,  1819,  T.  i. 

2  Mem.  de  la  Soc.  Med.  d'Obser.,  T.  iii,  p.  520. 

3  Klinik  der  Brustkrankheiten,  1874,  p.  254. 

4  Prager  Vierteljahrschrift,  10  Jahrg.,  Bd.  ii;   11  Jahrg.,  Bd.  ii. 

«  Handb.  d.  Path.  u.  Ther.  v.  Virchow,  1867,  v,  Bd.  i,  Abth.,  746. 

6  Scottish  Med.  and  Surg.  Jour.,  June,  1904. 

7  I  am  indebted  to  Dr.  F.  B.  Mallory  for  the  privilege  of  using  these  records. 


BRONCHIECTASIS  109 

in  early  childhood.  Among  Lebert's  83  cases,  15.6  per  cent,  occurred 
in  the  first  twenty  years  of  life,  32.4  per  cent,  from  twenty-one  to 
forty,  31.2  per  cent,  from  forty-one  to  sixty,  18  per  cent,  from  sixty- 
one  to  eighty,  and  2.4  per  cent,  from  eighty-one  to  eighty-five.  The 
cases  are  quite  evenly  divided  before  and  after  forty,  with  48  per  cent, 
for  the  former  and  52  per  cent,  for  the  latter  period.  In  King's  series 
of  64  cases,  53.1  per  cent,  occurred  between  twenty  and  forty  years.1 
As  might  be  expected,  the  age  at  death  is  lower  in  the  tuberculous 
cases,  being  ten  to  thirty  years  in  54.6  per  cent,  of  his  series. 

Males  are  more  frequently  affected,  comprising  55  per  cent,  of 
Lebert's  36,  and  77  per  cent,  of  King's  70  cases.  The  influence  of  the 
season  on  the  onset  is  difficult  to  determine  in  such  a  chronic  disease. 
Exacerbations  and  complications  are  more  frequent  in  the  colder 
months  of  the  year.  Thus  of  Lebert's  cases,  73  per  cent,  sought  the 
hospital  clinic  during  November  to  March,  only  27  per  cent,  from 
April  to  October. 

Clinical  Antecedents. — It  is  difficult  to  obtain  exact  data  on  the 
clinical  character  of  the  pulmonary  disease  from  which  bronchiectasis 
originates.  In  perhaps  a  majority  of  the  cases,  the  patients  are  unable 
to  recollect  any  striking  features  of  onset,  which  seems  to  have  been 
insidious.  In  a  second  group,  the  features  of  onset  are  those  of  an 
acute  and  apparently  mild  or  moderately  severe  respiratory  infection, 
which  may  start  in  any  part  of  the  tract  from  the  nose  to  the  bronchi, 
ultimately  invading  the  latter,  however,  and,  unlike  other  apparently 
similar  infections,  fails  to  resolve  after  the  customary  interval  of  a  few 
weeks.  In  such  cases  the  cough  and  purulent  sputum  persist.  Some 
of  these  patients  are  undoubtedly  already  the  subject  of  chronic 
respiratory  infection  of  the  nasopharyngeal,  the  bronchial  or  pulmonary 
tissue,  dating  from  a  previous  attack  which  has  not  wholly  subsided. 
In  them,  autoreinfections  are  superimposed  one  upon  another,  with 
successive  involvement  of  larger  and  larger  areas  and  increasing 
severity  of  symptoms.  In  their  clinical  aspect  alone,  such  cases  thus 
appear  to  take  their  origin  from  bronchitis.  It  is  improbable  that 
simple  bronchial  catarrh  is  a  sufficient  cause  for  bronchiectasis.  Bron- 
chial catarrh  alone  is  much  too  common  to  explain  so  infrequent  a 
disease,  and  a  special  type  of  bronchial  inflammation  present  in  only 
a  small  proportion  of  such  cases  must  be  assumed  to  exist.  Impaired 
resistance  of  the  bronchial  wall  itself,  in  consequence  of  the  infection, 
is  a  probable  explanation,  and  will  be  considered  more  fully  later. 

In  a  third  group,  pulmonary  disease  may  apparently  initiate  the 
condition.  In  this  class,  tuberculosis  appears  to  be  the  most  frequent 
cause.  It  was  present  in  21  (30.8  per  cent.)  of  Trojanowski's2  68  cases, 
in  22  (31.0  per  cent.)  of  King's  70  cases,  and  in  17  (37  per  cent.)  of 
my  45  cases.  The  tuberculosis  is  of  the  chronic  ulcerative  and  fibroid 
form  almost  without  exception.     In  rare  instances,   a  tuberculous 

1  Age  at  death.  2  Klin.  Beitrage  zur  Lehre  der  Bronchiectasie,  Dorpat,  1864. 


110  DISEASES  OF   THE   BROS  CHI 

bronchitis   may   coexist.     Bronchiectasis  may   take   its  origin    from 
unresolved  lobar  or  latent  or  obvious  bronchopneumonia. 

Bronchiectasis  may  follow  stenosis  of  the  bronchi  from  syphilitic 
or  tuberculous  ulceration,  new  growths  of  the  bronchial  wall,  pressure 
from  without  as  from  aneurysm  or  mediastinal  or  bronchial  tumor, 
and  the  inhalation  of  foreign  bodies. 

In  a  small  proportion  of  cases,  the  disease  follows  a  persistent  and 
usually  purulent  pleural  effusion,  which  has  perforated  the  lung  and 
thus  given  rise  to  pulmonary  and  bronchial  inflammation. 

Bacteriology. — Bacterial  infection  of  the  bronchial  wall  must  be 
regarded  as  the  underlying  cause  of  all  bronchial  dilatations.  The 
infection  may  be  primary  in  the  bronchi,  secondary  to  other  parts  of 
the  respiratory  tract  or  a  sequence  of  stenosis.  It  is  improbable 
that  the  disease  can  be  especially  ascribed  to  any  one  organism.  The 
influenza  bacillus,  Micrococcus  catarrhalis,  the  pneumococcal,  strep- 
tococcus, staphylococcus  and  the  tubercle  bacillus,  singly  or  combined, 
are  the  most  frequent  varieties  of  pathogenic  bacteria  found  in  the 
sputum  during  life,  or  in  the  lungs  after  death  in  these  cases.  Among 
18  cases  of  chronic  pulmonary  infection  with  influenza  bacilli  which  I 
studied  from  1902  to  1905,1  there  were  7  with  certain  or  probable 
bronchiectasis.  In  these  cases,  influenza  bacilli  were  in  practically 
pure  culture  in  the  sputum  over  a  long  period  of  observation  and  could 
fairly  be  regarded  as  the  cause  of  the  process.  Boggs2  in  1905,  reported 
6  cases  of  bronchiectasis  with  influenza  bacilli  in  practically  pure 
culture  in  the  sputum.  He  obtained  pure  cultures  of  influenza  bacilli 
at  autopsy  from  the  washed  and  teased  bronchial  wall  in  one,  and 
found  great  numbers  of  small  organisms  resembling  influenza  bacilli 
and  a  few  pneumococci  in  stained  sections  from  the  bronchial  wTall  in 
another. 

Pathology. — The  bronchial  dilatation  may  assume  various  shapes  in 
the  same  or  in  different  cases.  Among  these  the  cylindric,  fusiform, 
and  saccular  are  the  most  common.  Bead-like  or  moniliform  dilata- 
tion is  less  common.  Obliteration  of  afferent  and  efferent  bronchi 
may  convert  the  dilatation  into  a  cyst.  Club-  or  cone-shaped  dilata- 
tions may  also  be  seen.  The  size  of  the  dilatation  is  variable.  Ectasis 
of  the  smaller  tubes  may  give  rise  to  cavities  from  microscopic  dimen- 
sion to  that  of  a  pea  or  an  almond,  and  more  often  peripherally  placed, 
while  involvement  of  the  larger  bronchi  leads  to  cylindric  and  central 
dilatations  as  large  as  the  finger  or  thumb,  and  saccular  cavities 
the  size  of  a  walnut,  an  apple,  or  even  larger.  The  dilatation  of  com- 
municating bronchi  of  different  size  may  lead  to  tortuous  canalization 
of  the  lungs.  Dilatation  of  numerous  small  bronchi  may  convert  the 
lung  into  an  appearance  not  unlike  that  of  honeycomb.     The  bronchi 

1  F.  T.  Lord,  Eleven  Acute  and  Eighteen  Chronic  Cases  of  Influenza,  etc.,  Boston 
Med.  and  Surg.  Jour.,  December  18,  1902,  and  Infections  of  the  Respiratory  Tract 
with  Influenza  Bacilli  and  other  Organisms,  etc.,  ibid.,  May  11  and  IS,  1905. 

2  The  Influenza  Bacillus  in  Bronchiectasis,  Amcr.  Jour.  Med.  Sci.,  November,  1905. 


BRONCHIECTASIS  1 1  1 

emptying  into  bronchial  dilatations  are  often  obliterated.  In  rare 
instances  they  are  of  normal  size. 

Bronchiectasis  affects  one  bronchus  only  in  ran;  instances.  Thus 
of  45  cases  (Massachusetts  General  Hospital  and  Boston  ( !ity  Hospital 
series),  a  single  bronchiectatic  cavity  was  found  in  only  3,  all  of  which 
were  apical  and  tuberculous  in  origin.  Multiple  dilatations  may  be 
circumscribed  and  confined  to  one  lobe  as  in  5  of  this  series.  Multiple 
and  diffuse  lesions  are  far  more  common.  They  may  be  confined  to 
one  lobe,  as  in  10  cases  (22  per  cent.).  Among  Lebert's  54  cases,  15 
(27  per  cent.)  were  unilobar.  Unilateral  disease  is  recorded  in  52  per 
cent,  of  Lebert's  54,  and  37.7  per  cent,  of  King's  69  cases.  In  the 
presence  of  extensive,  multiple  lesions,  one  part  of  the  lung  is  likely 
to  be  more  extensively  involved.  In  general,  the  multiplicity  of  lesions 
is  one  of  the  most  striking  and  important  features  of  bronchiectasis. 
If  no  distinction  be  made  between  the  different  types  of  ectasis,  no 
striking  predilection  is  shown  for  any  particular  pulmonary  region. 
If  the  different  types  be  considered  separately,  certain  generalizations 
concerning  the  location  can  be  made.  Thus  tuberculous  bronchiec- 
tasis is  especially  likely  to  affect  one  or  both  apices  alone  or  predomi- 
nantly. In  17  tuberculous  cases  in  my  series,  the  bronchiectasis 
affected  one  or  both  apices  with  or  without  similar  lesions  elsewhere 
in  11.  In  these  cases,  the  most  pronounced  dilatation  is  usually  at  the 
apices.  In  non-tuberculous  bronchiectasis,  the  lower  lobes  are  affected 
in  a  somewhat  larger  proportion  than  in  the  tuberculous  cases.  Bron- 
chiectasis due  to  stenosis  from  syphilitic  ulceration,  pressure  from 
without  or  the  inhalation  of  foreign  bodies  is  more  likely  to  be  unilateral 
for  a  time  at  least. 

The  wall  of  the  dilated  bronchus  almost  constantly  shows  a  catarrh 
which  exists  also  in  undilated  bronchi,  with  an  increase  of  bronchial 
secretion.  The  mucous  membrane  is  usually  reddened.  In  exceptional 
instances  it  is  pale,  or  slate  colored.  The  bronchial  wall  may  be  thin, 
but  is  commonly  thickened,  firm  and  inelastic.  Its  surface  is  often 
uneven,  and  may  present  a  shaggy,  villous  appearance  not  unlike  that 
of  the  intestinal  villi.  In  advanced  cases,  intersecting  transverse  and 
longitudinal  ridges  of  elevated  tissue  may  convert  the  surface  into 
an  irregular  network  of  trabeculse.  Thin,  smooth-walled  dilatations 
are  sometimes  seen,  and  more  often  in  the  smaller  terminal  portions  of 
the  bronchi  unsupported  by  cartilage.  Erosion,  ulceration,  and  perfo- 
ration of  the  bronchial  wall  may  occur.  In  one  of  Lebert's  cases,  a 
perforation  involved  a  branch  of  the  pulmonary  artery  writh  fatal 
hemorrhage.  Suppurative  and  gangrenous  pulmonary  processes  may 
arise  in  consequence  of  perforation.  Calcareous  plates  may  be  found 
in  the  dilated  bronchi. 

On  microscopic  examination,  the  appearance  varies  with  the  stage 
of  the  disease.  In  early  processes,  the  mucous  membrane  is  uneven. 
The  bronchial  wall,  throughout,  is  rich  in  bloodvessels  and  shows  a 
striking  increase  in  small  round  cells.     Dilated  and  anastomosing 


112  DISEASES  OF  THE  BRONCHI 

vessels  are  especially  numerous  in  the  papillary  outgrowths.  Cellular- 
infiltration  is  seen  in  the  mucous  membrane,  about  and  between  the 

cartilages  and  glands,  about  and  within  the  muscular  and  elastic- 
layers.  The  epithelium  may  be  maintained,  or  partially  or  wholly 
detached.  In  later  stages,  proliferated  connective  tissue  may  partially 
or  wholly  replace  and  efface  the  characteristic  bronchial  structures. 
Invasion  and  compression  of  the  glandular,  muscular,  and  elastic 
elements  may  end  in  their  atrophy  and  ultimate  disappearance. 
Even  the  cartilages  are  gradually  diminished  in  size,  distorted,  and 
may  finally  disappear.  The  peribronchial  tissue  usually  participates 
in  the  indurative  process.  The  bronchial  wall  is  finally  converted  into 
a  thickened,  dense,  scar  tissue,  with  or  without  the  remnants  of  gland t 
ular,  muscular,  elastic,  and  cartilaginous  elements.  Invasion  of  the 
neighboring  alveolar  tissue  may  occur  to  a  variable  extent.  The  super- 
ficial layers  of  the  mucous  membrane  are  usually  spared.  A  thin 
layer  of  ciliated  epithelium  commonly  persists. 

The  differentiation  of  bronchiectasis  from  pulmonary  losses  of  sub- 
stance may  at  times  be  difficult  or  impossible.  The  following  features, 
however,  may  serve  to  distinguish  them.  Dilated  bronchi  are  likely  to 
present  a  smooth  and  shiny  surface,  in  unbroken  continuity  with  the 
mucous  membrane  of  undilated  portions  of  the  tube.  Microscopic 
examination  is  likely  to  show  ciliated  epithelium,  with  or  without 
glandular,  muscular,  elastic  and  cartilaginous  elements  or  their  rem- 
nants, in  more  or  less  typical  arrangement.  The  walls  of  pulmonary 
excavations,  on  the  other  hand,  are  usually  more  uneven,  shaggy  and 
distorted  from  unequal  losses  of  pulmonary  substance,  or  the  contrac- 
tion of  a  more  abundant  connective  tissue.  The  transition  from  normal 
bronchus  to  the  cavity  is  likely  to  be  more  abrupt.  As  pointed  out  by 
Virchow,1  the  relation  of  the  bloodvessels  to  the  cavity  is  an  important 
guide.  Careful  search  of  pulmonary  excavations  is  likely  to  disclose 
the  ends  of  eroded  vessels.  Beside  the  communicating  bronchus,  a 
place  may  usually  be  found  where  several  stumps,  easily  recognizable 
by  their  white  ends,  project  together  from  the  surface.  At  times  one 
can  plainly  distinguish  the  obliterating  thrombus  and  the  neighboring 
wall  of  the  vessel.  Partial  ulceration  of  the  wall  of  an  ectatic  bronchus 
may  be  a  cause  of  confusion. 

The  condition  of  the  pulmonary  tissue  is  very  variable.  It  is  prac- 
tically always  the  site  of  changes,  the  primary  or  secondary  relation 
of  which  to  the  bronchiectasis  is  often  difficult  to  determine.  In  one 
('98-250  B.C.H.)  among  45  cases,  the  bronchiectasis  was  apparently 
independent  of  any  pulmonary  affection.  The  bronchi  and  bronchioles 
were  dilated,  the  latter  reaching  as  much  as  1  cm.  in  diameter."  The 
lungs  showed  vesicular  emphysema  and  edema.  They  were  firmly 
bound  down  to  the  posterior  thoracic  wall  and  the  diaphragm  by  fibrous 
pleural  adhesions.    Death  was  due  to  chronic  endocarditis,  myocarditis, 

1  Verhandl.  der  Physikalisch-Modicinischen  Gosellschaft  in  Wurzburg,  Erlangen, 
1852,  Bd.  ii,  p.  24. 


BRONCHIECTASIS  113 

and  multiple  cerebral  hemorrhages.  It  is  not  uncommon  to  find 
dilated  bronchi  terminating  in  normal,  in  emphysematous  and  in 
diseased  pulmonary  tissue  in  the  same  lung.  Emphysema  is  off  en 
observed  and  may  be  local  or  diffuse.  It  was  present  in  1  I  of  Barth's 
40  cases  and  in  one  quarter  each  of  Biermer's1  and  Lebert's  series. 

Chronic  interstitial  pneumonia  is  common.  Jt  may  be  local  and 
limited  to  the  region  of  the  dilated  bronchi,  involving  principally  the 
peribronchial,  interlobular,  and  subpleural  connective  tissue.  M on- 
extensive  induration  may  convert  the  pulmonary  tissue  of  a  part  or  the 
whole  of  one  or  more  lobes  into  a  dense,  dry,  gray,  slate-colored  or 
even  black,  airless  mass  contracted  to  a  third,  one-half  or  even  more 
of  its  normal  volume,  and  in  which  the  dilated  bronchi  terminate 
blindly.  Acute  pneumonia  is  not  infrequent.  It  was  present,  as  a 
cause  of  death,  in  21  (!)  of  Rapp's2  24  cases.  Pneumonia  was  found  in 
12  of  Barth's  40  and  Biermer's  54  cases.  Lobar  pneumonia  was 
present  in  9,  and  bronchopneumonia  in  10  of  the  45  cases  in  my  series. 
Both  lobar  and  bronchopneumonia  may  initiate  or  complicate  bron- 
chiectasis. Pulmonary  abscesses  may  exist  independently  or  in  asso- 
ciation with  the  bronchial  dilatations.  Pulmonary  gangrene  was  a 
cause  of  death  in  5  of  Lebert's  cases. 

Pleuritis  is  almost  a  constant  finding.  It  is  rather  a  complication 
of  the  pulmonary  disease  with  which  the  bronchiectasis  is  associated 
than  of  the  bronchiectasis  itself.  Its  frequency  and  character  are  of 
interest  in  connection  with  the  question  of  surgical  interference.  In 
42  cases  in  my  series,  in  which  the  condition  of  the  pleura  was  noted, 
an  obliterating  pleurisy  was  found  over  both  lungs  in  8,  over  the 
involved  lung  in  9,  and  over  the  whole  of  that  part  of  the  lung  contain- 
ing dilated  bronchi  in  5.  The  pleural  sac  was  in  part  obliterated  over 
the  involved  region  in  5.  An  acute  fibrinous,  serofibrinous  or  purulent 
pleurisy  over  the  whole  or  a  part  of  the  affected  lung  was  found  in  5. 
Weak  bands  of  fibrous  adhesions  were  present  in  6  and  the  lungs  were 
free  in  4  cases.  Thus  in  32  cases  (76  per  cent.),  a  more  or  less  extensive 
pleurisy  coexisted  with  the  bronchiectasis.  The  pleurisy  often  forms 
the  outer  boundary  of  indurated  and  contracted  lung;  at  times  bands 
of  fibrous  tissue  of  variable  extent  connect  the  pleura  with  deep  or 
superficial  foci  of  pulmonary  induration,  or,  in  rare  instances,  the 
pleurisy  and  bronchiectasis  are  unassociated  with  changes  in  the  inter- 
vening pulmonary  substance.  Pleural  effusion,  when  it  occurs,  is 
likely  to  be  small  in  amount  and  limited  by  pleural  adhesions.  An 
abundant,  free  pleural  effusion  is  likely  to  occur  early,  if  at  all,  in  the 
course  of  bronchiectasis. 

Extrapulmonary  lesions,  secondary  to  the  bronchiectasis,  are  hard 
to  differentiate  from  those  which  develop  independently.    Hyperplasia 

1  Zur  Theorie  u.  Anat.  der  Bronchienerweiterung,  Virchow's  Arch.,  I860,  Bd.  xis, 
p.  160. 

2  Verhandl.   d.   Physik-med.   Gesellsch.   zu   Wiirzburg,   Sitzung    vom    25    Mai,    1S50, 
Bd.  i,  S.  145,  Erlangen  1850;  quoted  from  Bierraer. 


114  DISEASES  OF  THE  BRONCHI 

of  the  bronchial  lymph  glands  of  a  tuberculous  or  simple  character  is 
probably  the  most  common  extrapulmonary  complication.  Hyper- 
plasia of  the  spleen  is  not  infrequent  as  a  manifestation  of  toxemia 
or  terminal  septicemia.  Cerebral  abscesses  were  present  in  3  of  45 
rases.  Meningitis  occurred  in  7  instances.  It  was  tuberculous  in  1. 
Pericarditis  was  present  in  5  cases. 

Acute  or  chronic  endocarditis  is  not  infrequently  observed,  and  was 
noted  in  7  of  the  present  series.  It  may  take  its  origin  from  the  chronic 
bronchial  or  pulmonary  infection.  Cardiac  hypertrophy  and  dilatation, 
with  consecutive  chronic  passive  congestion  of  the  lungs,  the  liver, 
kidneys,  and  other  organs  may  be  ascribed  to  increased  pulmonary 
resistance,  in  the  absence  of  other  etiologic  factors.  Venous  throm- 
bosis occasionally  complicates  bronchiectasis  as  it  does  pulmonary 
abscess. 

Theories  of  Bronchiectasis. — Much  difference  of  opinion  has  pre- 
vailed concerning  the  explanation  of  bronchiectasis.  Biermer1  has 
reviewed  the  earlier  opinions.  The  different  theories  may  be  grouped 
under  three  principal  headings.  The  disease  has  thus  been  thought 
to  be  of  (1)  bronchial,  (2)  pulmonary,  or  (3)  bronchopulmonary  origin. 

1.  Bronchial  Theory. — Laennec  ascribed  the  dilatation  to  bronchial 
catarrh  and  stagnation  of  bronchial  secretion.  To  this  simple  explana- 
tion the  mechanical  effect  of  cough  and  a  disturbance  in  the  nutrition 
of  the  bronchial  wall  with  loss  of  elasticity,  contractility  and  ciliary 
motion  was  added  by  such  later  writers  as  Andral,2  Stokes,3  and  Wil- 
liams.4 Mendelsohn5  especially  emphasized  the  mechanical  effect  of 
forced  expiration,  with  the  glottis  closed  during  cough,  on  the  bronchial 
wall,  weakened  by  disease. 

2.  Pulmonary  Theory. — Corrigan6  believed  the  bronchial  dilatation 
to  be  due  solely  to  the  shrinkage  of  fibrotic  pulmonary  tissue  between 
the  bronchi,  the  diminished  pulmonary  volume  being  compensated 
either  by  thoracic  retraction  or  dilatation  of  unobliterated  bronchi. 

3.  Bronchopulmonary  Theory. — Hasse,7  Rokitansky,8  Engel,9  Riihle,10 
Biermer11  and  Lebert12  accepted  both  the  bronchial  and  pulmonary 
theories  in  whole  or  in  part,  with  varying  emphasis  on  one  or  the  other 
as  a  principal  factor. 

1  Zur  Theorie  u.  Anat.  d.  Bronchielerweiterung,  Virehow's  Archiv,  1860,  Bd.  xix. 

2  Clinique  med.,  etc.,  1824-27,  T.  W,  1st  ed.,  Paris;   2d  ed.,  1829. 

3  Diseases  of  the  Lungs  and  Windpipe,  Dublin,  1837. 

4  Lectures  on  the  Physiology  and  Diseases  of  the  Chest,  London,  1840,  4th  ed. 

6  Der  Mechanismus  der  Respiration  und  Circulation,  etc.,  Berlin,  1845,  p.  255  u.  ff. 

6  Dublin  Jour.,  May,  1838,  vol.  xiii,  No.  38. 

7  Anat.  Beschreibung  der  Krankheiten  der  Circulations-  und  Respirations-organe, 
Leipzig,  1841. 

8  Handbuch  der  path.  Anat.,  Wien,  1842,  Bd.  hi. 

9  Anleitung  z.  Beurtheilung  des  Leichenbefundes,  Wien,  1846. 

10  Untersuchungen  iiber  die  Hohlenbildungen  in  tuberculosen  Lungen,  Habilitations- 
dchrift,  Breslau,  1853. 

11  Zur  Theorie  und  Anatomie  der  Bronchielerweiterung,  Virehow's  Archiv,  1860, 
vol.  xix. 

12  Klinik  der  Brustkrankheiten,  1874,  vol.  i. 


BRONCHIECTASIS  115 

It  must  be  assumed  necessarily,  I  believe,  that  an  affection  of  the 
bronchial  wall  is  a  principal  factor  and  capable  alone  of  giving  rise  to 
dilatation.  Degenerative  changes  in  the  wall,  already  described  under 
Pathology,  are  constant,  and  may  be  unassociated  with  pulmonary 
disease,  thus  excluding  this  as  a  necessary  condition.  Simple  bronchial 
catarrh  is  much  too  common  to  explain  so  infrequent  a  disease  as 
bronchiectasis.  It  is  probable  that  in  a  certain  and  small  proportion 
of  cases  of  bronchial  infection,  the  infecting  agent  more  deeply  invades 
and  weakens  the  bronchial  wall.  The  stagnation  of  bronchial  secretion 
and  the  chronic  cough  with  increase  of  expiratory  pressure  within 
the  weakened  bronchi  may  then  easily  cause  dilatation.  Increase  of 
intrathoracic  pressure  under  muscular  strain  may  also  be  important. 
It  is  conceivable  that  unequal  distribution  of  negative  inspiratory 
pressure  may  unduly  inflate  certain  parts  of  a  lung  in  consequence  of 
focal  pulmonary  or  pleural  disease,  but  such  a  cause,  if  it  exists,  must 
play  but  a  minor  role,  and  would  affect  the  bronchi  in  normal  rather 
than  in  diseased  and  relatively  immobile  tissue.  The  extrabronchial 
traction  of  fibrotic  pulmonary  tissue,  as  an  accessory  factor,  cannot 
be  wholly  ignored.  Its  influence  is  probably  accidental,  at  times  serv- 
ing to  enlarge  or  distort,  at  other  times  to  diminish  the  size  of  ectatic 
cavities. 

Symptoms. — Cough  and  expectoration  are  the  principal  and  often 
the  only  symptoms.  The  cough  is  constant,  but  usually  much  aggra- 
vated in  the  winter  months.  In  the  early  period  of  the  disease  it  may 
almost  entirely  subside  during  the  summer,  to  reappear  with  the  onset 
of  cold  weather.  Acute  exacerbations  or  a  succession  of  "colds"  are 
likely  to  leave  the  patient  with  a  more  severe  cough.  In  some  cases, 
the  cough  lacks  distinctive  features,  but  in  the  majority  of  patients 
with  well-developed  bronchiectasis,  it  occurs  in  attacks,  with  relative 
or  complete  freedom  during  the  intervals.  The  number  of  attacks 
varies  from  one  to  several  or  more  in  the  twenty-four  hours.  The 
intermittent  character  of  the  cough  is  doubtless  due  to  insensitiveness 
of  the  diseased  and  dilated  bronchi.  The  incentive  to  cough  comes 
only  after  a  certain  degree  of  dilatation  is  reached  or  the  level  of  the 
accumulated  secretion  rises  to  a  more  healthy  bronchial  region.  A 
paroxysm  on  rising  in  the  morning  is  quite  constant,  and  is  due  to 
secretion  accumulated  during  the  night.  Recurrences  occur  during 
the  day  with  longer  or  shorter  periods  of  freedom.  The  attack  may 
last  from  a  few  minutes  to  a  half-hour  or  longer.  In  some  patients  the 
inclination  to  cough  comes  without  warning,  and  is  sudden  and  irre- 
sistible. In  one  of  my  series,  an  unexpected,  sudden  and  irresistible 
impulse  constantly  initiated  a  paroxysm,  in  which  several  ounces  of 
pus  were  forcibly  expelled  from  the  mouth  and  nose.  In  this  patient, 
partial  inversion  greatly  aided  the  evacuation  of  the  cavities.  The 
assumption  of  certain  positions  may  bring  on  a  paroxysm  of  cough. 
When  the  disease  is  unilateral,  longer  freedom  from  attacks  may  at 
times  be  secured  by  lying  on  the  affected  side,  thus  preventing  an 
overflow  of  secretion  into  healthy  bronchi. 


116  DISEASES  OF  THE  BRONCHI 

The  sputum  is  very  variable  in  amount.  From  100  to  200  c.c.  is 
not  uncommon  in  twenty-four  hours.  As  much  as  500  c.c.  or  more 
may  be  expectorated.  The  elimination  of  considerable  quantities 
("maulvolle"  expectoration  of  Wintrich)  with  each  cough  during  a 
paroxysm  may  be  a  striking  feature.  The  sputum  is  usually  muco- 
purulent or  purulent,  a  varying  shade  of  green,  and  slightly  tenacious 
from  the  presence  of  mucus  which  is  likely  to  adhere  to  separate 
masses,  thus  preventing  their  coalescence.  Even  in  severe  and  long- 
standing cases,  with  an  abundant  sputum,  the  expectorated  masses 
usually  remain  discrete  in  the  twenty-four-hour  specimen.  In  rare 
instances,  however,  an  almost  pure,  purulent  sputum  with  little 
admixture  of  mucus  may  be  observed  even  in  multiple  bronchiectasis. 
Such  homogeneously  purulent  specimens  are  seen  when  extensive 
degenerative  changes  have  occurred  in  the  bronchial  wall,  with  partial 
or  total  disappearance  of  the  mucous  glands.  The  expectoration  may 
be  odorless,  stale,  musty  or  foul.  In  rare  instances,  putrefaction  of 
the  secretion  within  the  bronchi  may  give  a  putrid  odor  to  the  breath 
and  the  sputum  in  the  absence  of  pulmonary  gangrene.  On  standing, 
the  sputum  usually  separates  into  three  layers  such  as  are  described 
under  Pulmonary  Abscess  and  Gangrene.  Dittrich's  plugs  (see  Abscess 
and  Gangrene)  may  be  found. 

Hemoptysis  occurs  in  about  equal  frequency  in  tuberculous  and  in 
non-tuberculous  bronchiectasis.  It  was  present  in  45.1  per  cent,  of 
King's  62  cases.  A  distinction  of  some  clinical  value  may  be  made 
between  those  hemorrhages  which  come  early  and  those  which  occur 
late  in  the  course  of  the  disease.  As  an  initial  symptom,  or  early  in  the 
course  of  an  apparently  mild  pulmonary  disturbance,  the  hemoptysis 
is  likely  to  be  tuberculous  in  origin.  When  it  occurs  in  association 
with  other  symptoms,  among  which  an  abundant  purulent  sputum 
is  a  prominent  feature,  tuberculosis,  although  frequent,  is  less  often 
a  cause.  The  blood  occurs  in  streaks  or  as  moderate,  profuse  or  fatal 
hemorrhage,  as  in  3  (4.8  per  cent.)  of  King's  cases.  Small  amounts 
of  blood  come  from  the  vascular,  papillary  outgrowths  in  the  walls  of 
the  bronchi,  denuded  of  epithelium.  More  abundant  hemorrhages 
may  come  from  rupture  of  branches  of  the  pulmonary  artery  by  erosion 
of  the  bronchial  wall.  In  some  instances,  bloodvessels  lining  the  wall 
or  traversing  the  lumen  of  pulmonary  cavities  are  the  source.  It 
is  at  times  impossible  to  determine  the  origin  of  the  bleeding. 

Pain,  when  it  occurs,  is  usually  due  to  complicating  pleurisy.  Dysp- 
nea is  not  a  prominent  symptom,'  in  most  cases.  It  may  occur  in 
attacks,  and  the  clinical  picture  may  be  that  of  bronchial  asthma 
complicating  bronchiectasis. 

Physical  Signs. — The  general  nutrition  is  usually  little  disturbed. 
Slight  cyanosis  of  the  lips,  the  hands  and  feet  is  common.  It  is  likely 
to  be  marked  after  a  paroxysm  of  cough.  Dilatation  of  the  jugular 
veins  is  also  at  times  observed.  The  skin  may  be  dry.  Chills  may 
occur  if  there  is  retention  of  secretion.     The  temperature  is  usually 


BRONCHIECTASIS  117 

unelevated,  when  the  discharge  of  pus  is  unobstructed  and  in  the 
absence  of  complications.  Transient,  irregular,  intermittent  or  remit- 
tent fever,  however,  may  be  due  to  stagnant  secretion,  an  acute  exacer- 
bation of  the  chronic  infection,  or  extension  of  the  disease  to  previously 
uninvolved  parts  of  the  bronchi  or  lung,  giving  rise  to  acute  bronchitis, 
broncho-  or  lobar  pneumonia,  abscess,  gangrene  or  pleurisy.  The 
pulmonary  signs  present  important  differences  in  the  purely  bronchial 
and  the  bronchopulmonary  form. 

Pure  Bronchiectasis. — This  comprises  only  a  very  small  proportion 
of  the  cases.  As  has  been  noted  under  Pathology,  bronchial  dilatation 
is  only  very  rarely  unassociated  with  pulmonary  or  pleural  disease. 
The  pulmonary  process,  however,  is  not  infrequently  focal  or  deep 
seated,  and  may  thus  readily  escape  detection.  It  happens,  therefore, 
that  pure  bronchiectasis  appears  to  be  less  frequent  clinically  than 
is  actually  the  case.  In  this  form,  there  are  often  no  pulmonary  signs 
whatever,  even  when  there  is  a  large  amount  of  sputum.  Coarse, 
medium  or  fine,  non-consonating  rales  may  at  times  be  heard.  They 
are  likely  to  be  variable  in  character  and  occurrence,  present  at  one, 
absent  at  another  examination.  They  may  disappear  after  evacuation 
of  the  cavities  in  a  paroxysm  of  cough.  Persistent  localization  at  one 
or  several  places  in  one  or  both  lungs  may  suggest  the  site  of  the 
disease. 

Bronchopulmonary  Form. — This  comprises  a  large  proportion  of  the 
cases.  The  physical  signs  are  very  variable.  If  the  pulmonary  disease 
is  of  slight  extent,  the  signs  may  be  limited  to  rales,  which  are  almost 
constantly  present.  They  may  be  fine,  medium,  or  coarse  and  conso- 
nanting  or  non-consonating.  In  the  presence  of  extensive  or  superficial 
pulmonary  induration  or  bronchopneumonia,  there  may  in  addition 
be  dulness,  bronchial  breathing,  increase  of  voice,  whisper,  and  tactile 
fremitus.  The  bronchial  cavities  may  be  indicated  by  a  dull  tym- 
panitic note  on  percussion,  changes  in  the  quality  of  the  note  when 
the  patient's  mouth  is  open  and  closed,  and  on  shifting  the  patient's 
position,  cracked-pot  percussion  note,  bronchial  and  amphoric  breath- 
ing and  marked  increase  in  the  voice,  whisper,  and  tactile  fremitus. 
A  difference  in  the  signs  before  and  after  evacuation  of  the  cavities  is 
also  suggestive.  Distinctive  physical  signs  of  bronchial  dilatation, 
however,  are  often  absent  and  the  location  of  the  process  may  depend 
upon  the  site  of  the  associated  pulmonary  disease.  Extensive  unilateral 
or  predominantly  unilateral  pulmonary  or  pleuropulmonary  fibrosis 
may  cause  restricted  respiratory  motion,  thoracic  retraction  and  nar- 
rowing of  the  intercostal  spaces  over  the  affected  region.  There  may 
also  be  lateral  deviation  of  the  spine  and  dislocation  of  the  heart  toward 
the  involved  area.  If  pleural  thickening  is  marked,  it  may  mask  the 
signs  of  the  underlying  pulmonary  and  bronchial  disease. 

Varying  degrees  of  emphysema  are  likely  to  complicate  both  forms 
of  bronchiectasis.  If  it  is  marked,  it  may  introduce  striking  features 
into  the  physical  examination.    There  may  be  round  shoulders,  barrel 


L18  DISEASES  OF  THE  BRONCHI 

chest,  prominent  clavicles,  sternum  and  costal  cartilages,  diminished 
inspiratory  excursion,  invisible  and  impalpable  apex  beat,  hyper- 
resonance  on  percussion,  partial  or  complete  obliteration  of  the  super- 
ficial cardiac  dulness,  displacement  downward  of  the  upper  level  of 
the  hepatic  and  splenic  dulness,  and  on  auscultation,  feeble  breathing 
and  prolonged  expiration. 

Complications. — These  have  already  been  considered  under  Path- 
ology. In  their  clinical  aspects,  certain  complications  deserve  further 
mention.  Acute  bronchopneumonia  arising  by  extension  or  aspira- 
tion is  common.  It  may  be  indicated  clinically  merely  by  an  increase 
of  the  cough  and  expectoration,  the  appearance  of  rales  in  a  region 
previously  uninvolved,  or  evidence  of  a  more  severe  or  extensive  Ideal 
lesion.  Varying  degrees  of  general  disturbance  and  fever  are  likely 
to  accompany  the  attacks.  The  neighborhood  of  the  already  existing 
bronchial  or  bronchopulmonary  lesions  is  most  likely  to  be  affected, 
but  infection  of  more  remote  areas  also  occurs.  It  is  usually  found 
that  the  extent  of  the  bronchopulmonary  disease  is  increased  after  the 
attack.  Lobar  or  bronchopneumonia  may  be  a  terminal  event  or  end 
in  partial  or  complete  resolution.  Pulmonary  abscess  is  a  frequent 
complication.  Gangrene  also  occurs.  Intercurrent  attacks  of  pleurisy 
are  common.  They  are  usually  unaccompanied  by  effusion.  In  some 
cases  the  symptoms  of  pleurisy  dominate  the  clinical  picture.  An 
effusion  may  be  putrid,  as  in  3  of  7  cases  of  empyema  complicating 
bronchiectasis  in  Frankel's  series.  Cerebral  abscess  and  meningitis, 
probably  arising  by  metastasis,  are  not  infrequent.  Hypertrophic 
osteo-arthropathy  is  more  frequently  associated  with  bronchiectasis 
than  with  other  pulmonary  conditions. 

Hypertrophic  "Pulmonary"  Osteo-arthropathy. — This  interesting  con- 
dition was  first  described  by  Bamberger1  and  Marie.2  Simple  clubbing 
of  the  fingers  and  toes,  frequently  noted  in  patients  with  chronic 
pulmonary  and  cardiac  disease  (especially  congenital  cases),  may  for  the 
present  be  regarded  as  an  early  or  mild  form  of  Marie's  disease.  Only 
those  cases  in  which  the  clubbing  is  associated  with  bony  changes 
should  be  classed  in  this  group. 

Hypertrophic  osteo-arthropathy  is  commonly  associated  with  chronic 
pulmonary  or  pleural  disease,  as  in  65  (69  per  cent.)  of  Janeway's3 
93  cases.  Bronchiectasis4  is  the  most  common  pleuropulmonary  con- 
dition, and  was  present  in  20.  Pulmonary  tuberculosis  with  cavity 
formation  was  recorded  in  14  cases.  Chronic  bronchitis,  abscess,  pul- 
monary tuberculosis  without  cavities,  chronic  pleurisy  or  pneumonia 
and  malignant  disease  of  the  pleura  have  also  been  reported.  The 
disease  may  be  coincident  with  such  other  conditions  as  hypertrophic 

1  Wiener  klin.  Woch.,  1889,  p.  225,  and  Zeit.  f.  klin.  Med.,  1891,  Bd.  xviii,  p.  193. 

2  De  l'osteoarthropathie  hypertrophiante  pneumique,  Rev.  de  med.,  1890,  x,  1. 

3  Amer.  Jour.  Med.  Sei.,  1903,  exxvi,  574. 

4  v.  Criegern  (Ueber  akute  Bronchiektasie,  etc.,  Leipzig,  1903)  noted  swelling  of  the 
terminal  phalanges  in  18  of  35  cases  of  bronchiectasis. 


BRONCHIECTASIS  119 

cirrhosis  (with  jaundice),  syphilis,  valvular  cardiac  lesions,  cancer 
of  the  esophagus,  sarcoma  of  the  parotid,  chronic  dysentery,  chronic 
alcoholism,  acute  pneumonia  and  influenza,  thus  indicating  that  pul- 
monary lesions  are  not  a  necessary  association  and  that  the  term 
"pulmonary"  hypertrophic  osteoarthropathy  of  Marie  is  inapplicable 
to  all  cases.  In  a  small  proportion  of  cases,  the  disease  is  apparently 
an  independent  affection,  the  patients  being  otherwise  healthy  or 
developing  other  lesions  in  the  course  of  the  process.  The  use  of  the 
term  "secondary,"  as  in  Arnold's1  secondary  hyperplastic  ostitis,  is 
therefore  also  inappropriate.  It  occurs  in  both  sexes,  but  much  more 
commonly  in  the  male,  the  relation  of  male  to  female  in  Wynn's2 
series  being  83  to  11.  No  age  is  exempt.  Most  cases  occur  between 
the  ages  of  twenty  and  sixty.  The  cause  of  the  disease  is  unknown. 
The  absorption  of  toxic  substances,  of  an  uncertain  character,  and 
venous  stasis,  singly  or  combined,  are  possible  explanations. 

The  disease  is  characterized  by  symmetrical  enlargement  of  the 
hands  and  feet.  Clubbing  of  the  fingers  and  toes  is  a  striking  feature. 
All  the  digits  are  affected.  The  thumb,  index,  and  middle  fingers 
are  likely  to  be  most  markedly  involved.  The  enlargement  is  both 
anteroposterior  and  lateral,  and  gives  to  the  finger  a  drumstick 
appearance.  Swelling  of  the  interphalangeal  joints  may  give  a  spindle 
shape  as  well  to  the  fingers.  The  nails  are  wider  and  longer  than  normal, 
curved  like  a  parrot's  beak,  show  longitudinal  striation,  and  may  be 
brittle  and  cyanotic.  Pressure  on  the  distal  extremity  of  the  nail 
tilts  the  proximal  part  with  the  formation  of  a  ridge  on  the  dorsal 
surface.  Similar  but  less  striking  changes  are  seen  in  the  toes.  The 
hands  may  be  widened  from  thickening  of  the  metacarpal  bones. 
In  addition,  there  may  be  thickening  of  the  distal  ends  of  the  bones 
of  the  forearm  and  leg.  Enlargement  of  the  lower  end  of  the  humerus 
and  femur  is  at  times  also  observed.  In  extreme  cases,  the  outer  third 
of  the  clavicle,  the  acromium  process  and  spine  of  the  scapula,  the 
ribs,  iliac  crests  and  patella  may  also  be  affected.  Posterior  and  lateral 
curvature  of  the  spine  and  enlargement  of  the  spinous  processes  have 
been  observed.  The  wrists,  ankles  and  knees  may  be  stiff  and  swollen. 
The  shoulders,  elbows,  and  small  joints  of  the  hands  and  feet  are  at 
times  similarly  affected.  The  ankles  may  pit  on  pressure.  The  tip 
of  the  nose  may  be  globular  and  the  malar  prominences  abnormally 
developed. 

The  skin  over  the  affected  regions  may  be  stretched  and  shiny  from 
obliteration  of  the  normal  furrows  and  depressions.  Some  muscular 
atrophy,  especially  of  the  arms,  is  occasionally  observed.  Pain  is 
usually  absent,  but  discomfort  or  pain  and  tenderness  may  occur 
when  the  disease  is  rapidly  progressing  or  during  an  exacerbation. 
The  blood  shows  nothing  characteristic. 


1  Ziegler's  Beitrage  z.  Path.  Anat.  u.  z.  allg.  Path.,  1891,  x,  1. 

2  Birmingham  Med.  Rev.,  1904,  vol.  lv. 


120  DISEASES  OF  THE  BRONCHI 

Postmortem  examination  of  the  affected  regions  has  been  made  by 
Bamberger,1  Lefevre,2  Therese,3  Rauzier,1  and  Thorburn.5  The 
affected  bones  show  periosteal  thickening  with  the  formation  of  new 
bone  in  the  deeper  layers.  Irregular  bony  deposits  may  give  the  bone 
an  irregular  outline  or  form  definite  osteophytes.  These  are  most 
abundant  in  the  region  of  the  epiphysis.  The  cortical  bone  is  thickened 
and  the  process  may  thus  be  termed  an  osteoperiostitis  ossificans. 
The  medulla  is  diminished  in  size,  rarefied  and  more  fatty  than  normal. 
The  joints  may  show  both  thickening  of  the  synovial  membranes  and 
erosion  of  the  articular  cartilages,  with  an  excess  of  fluid.  The  clubbing 
of  the  fingers  is  due  to  swelling  of  the  soft  parts  and  not  bony  enlarge- 
ment, both  in  simple  clubbing  and  that  associated  with  Marie's  disease. 

The  onset  is  usually  slow  and  insidious,  but  may  be  rapid.  West6 
reports  the  development  of  clubbing  of  the  fingers  within  a  fortnight 
and  four  weeks  respectively.  As  a  complication  of  pulmonary  or 
other  lesions,  the  disease  usually  develops  within  six  months  to  a  year 
of  the  onset  of  the  associated  condition.  Its  appearance  may  be  delayed 
for  from  four  to  ten  years.  In  rare  instances,  its  onset  coincides  with 
or  even  precedes  the  manifestations  of  the  other  lesions.  The  course 
is  usually  slowly  progressive.  Acute  exacerbations  are  occasionally 
observed.  In  rare  instances,  improvement  has  been  noted.  Moderate 
diminution  in  the  size  of  the  soft  tissue  was  observed  in  osteoarthrop- 
athy within  two  months  by  Schittenhelm.7  Improvement  has  been 
noted  after  cure  of  the  primary  disease  by  Godlee8  and  by  Metten- 
heimer.9  Marked  improvement  of  simple  clubbing  of  the  fingers 
secondary  to  empyema  has  been  noted  by  Moussons,19  complete  dis- 
appearance by  Gillet11  and  Moizard.12 

Diagnosis. — This  is  difficult.  Bronchiectasis  should  be  suspected 
in  the  presence  of  long-continued  cough  with  abundant,  mucopurulent 
or  purulent  sputum,  expectorated  in  attacks,  with  relative  or  complete 
freedom  during  the  intervals.  Similar  symptoms  occur  also  in  chronic 
pulmonary  abscess  and  gangrene,  occasionally  also  in  interlobar, 
diaphragmatic  or  ordinary  pleural  empyema,  breaking  through  the 
lung  into  the  bronchi.  Inasmuch  as  dilatation  of  the  bronchi  may 
occur  in  the  course  of  any  long-continued  pulmonary  suppuration  and 
be  present  without  characteristic  symptoms,  it  should  be  kept  in  mind 
as  a  possibility  in  any  chronic  cough  with  purulent  expectoration. 

1  Loc.  cit. 

2  Des  deformations  osteoarticulaire  consecutives  a  des  maladies  de  l'appareil  pleuro- 
pulmonaire  (osteoarthropathie  hypertrophiante  de  Marie),  These,  Paris,  1891. 

3  Bull,  de  la  Soc.  anat.  de  Paris,  1891,  p.  143.  4  Rev.  de  med.,  1891. 
6  Thorburn  and  Wcstmacott,  Path.  Trans.,  vol.  xlvii,  p.  177. 

6  Two  Cases  of  Clubbing  of  the  Fingers  Developing  within  a  Fortnight  and  Four 
Weeks  Respectively,  Clin.  Soc.  Trans.,  1897,  vol.  xxx. 

7  Berl.  klin.  Woch.,  1902,  xxxix,  2.54.  8  British  Med.  Jour.,  1896,  ii,  57. 
9  Zeit.  f.  rationelle  prak.  Acrzte,  1885,  p.  449. 

10  Jour,  de  med.  de  Bordeaux,  1890. 

11  Annales  de  la  polielinique  de  Paris,  1892,  ii,  93. 

12  Bull,  et  mem.  Soc.  Med.  des  Hop.  de  Paris,  1893,  ser.  3,  x,  359. 


BRONCHIECTASIS  121 

Acute  losses  of  pulmonary  substance  (abscess  and  gangrene)  are 
usually  readily  excluded  by  the  short  period  which  elapses  between 
the  onset  of  symptoms  and  the  appearance  of  purulent  sputum,  the 
intensity  of  the  general  disturbance  and  fever,  the  signs  of  cavity,  if 
present,  and  the  presence  of  elastic  tissue  and  shreds  of  pulmonary 
tissue  in  the  expectoration.  Chronic  pulmonary  excavations  cannot 
be  differentiated  with  certainty.  The  absence  of  signs  of  pulmonary 
disease  may  suggest  bronchiectasis.  Such  positive  features  as  the 
finding  of  tubercle  bacilli,  actinomyces,  or  elastic  tissue  with  an  alveolar 
arrangement,  are  certain  evidence  of  pulmonary  destruction,  but  do 
not  exclude  a  complicating  bronchiectasis.  The  absence  of  tubercle 
bacilli  or  elastic  tissue  is  of  little  moment  in  the  differential  diagnosis 
between  chronic  abscess  and  bronchiectasis.  Inactivity  of  the  pul- 
monary process  may  account  for  their  absence  in  abscess.  The  signs 
of  cavity  are  more  likely  to  indicate  losses  of  pulmonary  substance 
than  dilated  bronchi. 

A  long-neglected  empyema  perforating  the  lung  may  be  a  cause  of 
confusion.  Uncertainty  between  empyema  and  bronchiectasis  is  not 
likely  to  exist  when  the  rupture  into  the  lung  is  sudden  and  followed 
by  the  expectoration  of  a  large  amount  of  clear  pus,  but  in  the 
more  latent  cases,  in  which  pus  slowly  finds  its  way  through  single 
or  multiple  channels  from  the  pleura  to  the  bronchi.  If  the  patient 
comes  under  observation  only  after  considerable  pulmonary  damage  has 
occurred,  the  case  may  appear  to  be  one  of  bronchiectasis  of  the  broncho- 
pulmonary form  with  a  complicating  pleurisy.  In  such  instances  the 
history  may  be  suggestive.  Cough  and  abundant  sputum  are  likely 
to  antedate  the  onset  of  pleurisy  secondary  to  bronchiectasis.  In 
empyema  perforating  the  lung,  the  pleural  precede  the  pulmonary 
symptoms.  Ordinary  empyema  is  usually  readily  detected  on  physical 
examination.  Ruptured  interlobar  empyema  which  fails  to  reach 
the  chest  wall  may  be  suggested  by  dislocation  of  the  heart,  physical 
signs  in  the  region  of  the  interlobar  septa  and  a>ray  examination. 
Evacuation  into  the  lung  of  an  abscess  between  lung  and  diaphragm 
may  be  preceded  by  symptoms  of  diaphragmatic  pleurisy,  dislocation 
of  the  heart,  the  diaphragm,  and  with  it  the  liver  or  spleen  downward 
and  x-ray  examination. 

The  determination  of  the  cause  of  the  bronchiectasis  may  be  diffi- 
cult. Tuberculosis  is  the  underlying  cause  in  about  one-third  of  the 
cases.  A  family  history  of  the  disease  or  known  opportunity  for  con- 
tagion, loss  of  weight  and  strength,  night-sweats,  fever,  hemoptysis 
or  pleurisy  as  an  initial  symptom  or  early  in  the  course  of  the  disease, 
apical  involvement,  and  a  reaction  to  tuberculin  suggest  tuberculosis. 
Tubercle  bacilli  should  be  diligently  and  repeatedly  sought.  Their 
absence  from  an  abundant  purulent  sputum  is  important,  but  hot 
conclusive  evidence  against  tuberculosis.  Bronchiectasis  and  fibroid 
phthisis,  with  an  abundant  purulent  sputum,  may  still  exist  without 
tubercle  bacilli  in  the  sputum.    Such  a  process  may  be  at  the  base  of  the 


122  DISEASES  OF   THE  BROS  CHI 

lung  and  due  to  tuberculosis,  as  shown  by  postmortem  examination. 
In  general,  it  may  be  said  that  the  duration  of  life  is  shorter  in  the 
tuberculous  than  in  the  non-tuberculous  cases,  but  this  is  of  little 
moment  in  deciding  the  character  of  the  individual  infection. 

Syphilitic  stenosis  as  a  cause  may  be  suggested  by  the  history,  the 
rinding  of  tracheal  and  bronchial  ulcerations  on  bronchoscopic  exami- 
nation, the  presence  of  syphilitic  lesions  elsewhere,  or  a  positive  Wasser- 
nianii  test.  A  foreign  body  should  be  considered.  It  may  have  been 
unconsciously  inhaled  and  first  disclosed  by  .r-ray  examination.  The 
diagnosis  of  pressure  from  aneurysm  or  mediastinal  growth  is  usually 
easily  made  from  the  history,  the  physical  signs  and  .r-ray  examination. 

X-ray  Examination. — This  is  of  less  value  than  in  pulmonary  abscess 
and  gangrene.  It  is  of  principal  service  in  disclosing  the  presence  of 
pulmonary  changes.  Little  if  any  assistance  can  be  expected  from  it 
in  the  cylindric  form  of  the  disease.  In  the  saccular  ectasies,  a  rela- 
tively less  dense  shadow  may  be  observed  in  the  midst  of  an  involved 
region.  Comparison  of  plates  taken  before  and  after  evacuation  of  the 
bronchial  dilatations  may  be  very  suggestive.  A  shadow  on  a  plate 
taken  before  evacuation  may  disappear  or  show  more  translucent 
areas  after  evacuation.  As  in  pulmonary  abscess  and  gangrene,  .r-ray 
examination  may  be  an  important  guide  for  surgical  interference. 

Exploratory  Puncture. — This  is  inadvisable  for  the  reasons  given 
under  Pulmonary  Abscess  and  Gangrene. 

Prognosis. — Restoration  of  the  bronchi  to  normal  cannot  be  expected. 
The  disease  runs  a  very  chronic  course,  subject  to  exacerbations  and 
remissions.  The  duration  varies  in  different  cases  and  according  to 
the  cause.  Bronchiectasis,  which  complicates  aneurysm  or  medias- 
tinal new  growth,  may  unfavorably  influence  the  already  grave  out- 
look in  these  affections  and  shorten  their  course.  The  prognosis  of 
tuberculous  bronchiectasis  is  worse  than  in  the  non-tuberculous  form, 
but  is  in  general  somewhat  more  favorable  than  in  ordinary  pulmonary 
tuberculosis,  since  the  condition  is  more  likely  to  be  associated  with  the 
fibroid  form  than  with  other  types  of  phthisis.  The  duration  of  41 
cases  of  non-tuberculous  bronchiectasis  (King)  arising  in  consequence 
of  bronchial,  pulmonary  or  pleural  disease  was  three  to  ten  or  more 
years  in  46.2  per  cent.  In  itself  the  disease  is  not  incompatible  with 
a  long  term  of  life,  but  is  a  constant  menace  to  the  individual  as  a 
source  of  infection  of  nearby  or  remote  parts  of  the  body.  Broncho- 
pneumonia, abscess,  gangrene,  empyema,  pneumothorax,  cerebral 
abscess  and  meningitis  may  be  mentioned  as  among  the  most  serious 
complications.  Emphysema  and  interstitial  pneumonia  may  be  the 
cause  of  cardiac  insufficiency.  Amyloid  may  follow  long-continued 
bronchial  or  bronchopulmonary  suppuration.  In  rare  instances, 
hemoptysis  may  be  fatal. 

Prophylaxis. — The  constant  presence  in  the  abundant  sputum  of 
patients  with  bronchiectasis  of  such  organisms  as  the  influenza  bacillus, 
the  pneumococcus,  the  pyogenic  cocci,  Micrococcus  catarrhalis,  tubercle 


BRONCHIECTASIS  123 

bacilli  and  others,  singly  or  combined,  must  be  regarded  as  a  menace, 
not  only  to  the  patient  himself,  but  also  to  others  in  his  neighborhood. 
These  chronic  carriers  of  infection  may  well  serve  as  a  source  of  con- 
tagion by  their  constant  output  of  innumerable  pathogenic  bacteria. 
This  applies  to  the  non-tuberculous  as  well  as  to  the  tuberculous  cases, 
and  the  same  control  should  be  exercised  over  both  groups. 

The  patient  should  be  made  to  understand  that  his  sputum  is  a 
danger  to  others,  and,  if  allowed  to  dry,  may  be  capable  of  spreading 
disease.  It  should  be  carefully  expectorated  into  a  special  receptacle 
to  avoid  soiling  the  beard  or  moustache.  In  coughing  or  sneezing, 
expelled  particles  should  be  caught  in  a  piece  of  cloth  placed  in  front 
of  the  mouth.  These  should  be  burned.  The  fingers  should  not  be 
moistened  in  the  mouth  in  turning  the  leaves  of  books,  public  docu- 
ments, etc.  The  table  utensils  may  well  be  kept  separate  from  those 
of  other  members  of  the  family.  Soiled  bed  and  body  linen  should 
be  boiled.  Dusting  the  patient's  room  should  be  done  with  a  dampened 
cloth,  sweeping  with  a  dampened  broom.  The  patient  should  sleep 
alone.    An  abundance  of  sunlight  and  fresh  air  limit  the  danger. 

Instruction  should  be  given  in  the  best  method  of  disposal  of  sputum. 
The  safest  is  by  cremation.  Carbolic  acid  (5  per  cent.)  is  the  most 
efficient  of  the  ordinary  disinfectant  solutions  and  should  be  left  in 
contact  with  the  sputum  for  twenty-four  hours. 

For  the  patient  himself,  certain  measures  may  limit  the  danger  of 
auto-infection  or  reinfection.  The  sputum  should  not  be  swallowed. 
The  patient  should  be  especially  careful  to  avoid  exposure  to  wet  and 
cold,  and  rapid  cooling  of  the  body  after  exertion.  Thin  woolen  under- 
wear and  an  effort  to  increase  individual  resistance  may  afford  some 
protection.  Sleeping  with  the  window  open,  spending  much  time  in 
the  open  air  and  cool  bathing  followed  by  friction  are  helpful.  A  good 
reaction  should  be  secured  after  the  bath. 

Treatment. — 1.  General. — Every  effort  should  be  made  to  improve 
the  nutrition  and  maintain  it  at  a  high  level.  An  abundance  of  food, 
extra  feedings  and  fresh  air  by  night  as  well  as  by  day  are  of  assistance. 
Patients  with  bronchiectasis  are  usually  strikingly  better  during  the 
warm  months  of  the  year.  Their  condition  is  improved  by  an  out- 
door life  in  a  warm,  equable  climate  and  in  an  atmosphere  free  from 
dust. 

2.  Special. — An  attempt  is  made  by  various  means  to  disinfect  and 
more  completely  evacuate  the  bronchi.  It  is  unlikely  that  disinfection 
can  be  accomplished  with  safety  by  any  means  whatsoever.  Any 
improvement  which  follows  the  attempt  thus  to  control  the  disease 
must  be  ascribed  to  the  more  complete  evacuation  of  the  bronchial 
secretion  by  the  more  vigorous  paroxysms  of  cough  following  irrita- 
tion of  the  bronchial  mucous  membrane. 

(a)  Inhalations. — Owing  to  the  increased  respiratory  excursion  of 
sound  parts  of  the  lungs,  a  larger  part  of  the  inhaled  substance  may  be 
expected  to  reach  the  normal  than  the  diseased  bronchi.    The  inhala- 


124  DISEASES  OF   THE  BRONCHI 

tions  are  troublesome.  An  improvement  in  the  cough  and  a  diminution 
in  the  amount  of  expectoration  is  at  times  observed.  The  vapor  of 
oil  of  turpentine  (a  teaspoonful  to  the  pint  of  boiling  water)  may  be 
used.  The  fumes  of  creosote  may  be  inhaled.1  A  small  air-tight  room 
is  used  for  the  inhalation.  The  creosote  is  placed  in  a  flat,  open  dish, 
heated  by  means  of  a  spirit  lamp.  Gas  should  not  be  used,  unless 
conducted  to  the  burner  by  a  metal  tube.  Rubber  tubing  may  be 
ignited  by  burning  creosote,  which  overflows  the  sides  of  the  dish. 
The  spirit  lamp  should  be  placed  in  a  large  flat,  open  metal  vessel. 
The  patient's  eyes  are  protected  from  the  irritating  effect  of  the  fumes 
by  two  watch  glasses  framed  with  adhesive  plaster;  the  nose  by  plugs 
of  absorbent  cotton.  Saturation  of  the  hair  and  clothing  may  be  pre- 
vented by  a  towel  about  the  scalp  and  a  dressing  gown.  Treatment  is 
taken  daily  for  twenty  minutes  to  an  hour  or  longer.  Carbolic  acid 
(2  to  4  per  cent.)  or  thymol  (2  to  4  per  cent.)  may  also  be  inhaled. 
Vaporization  may  be  accomplished  by  means  of  an  inhalation  appara- 
tus, of  which  there  are  many  models  on  the  market.  Simple  normal 
salt  solution  may  be  similarly  used.  Ten  drops  or  more  of  a  solution  of 
liquid  carbolic  acid  or  thymol,  rectified  spirit  and  glycerin,  equal  parts 
of  each,  may  be  dropped  upon  a  face-mask  and  thus  inhaled.  They 
may  disguise  a  foul  odor  of  the  breath. 

(b)  Intratracheal  Injections. — Menthol,  iodoform  or  eucalyptol  (10 
per  cent.)  in  olive  oil,  a  dram  of  which  is  injected  once  or  twice  a  day 
through  the  glottis  by  means  of  a  syringe  with  a  curved  nozzle,  is  some- 
times used.  Granger  Stewart2  recommends  menthol  10  parts,  guaiacol 
2  parts,  olive  oil  88  parts. 

(c)  Internal  Medication. — This  is  unsatisfactory.  Ammonium 
chlorid  gr.  10  (0.65  gm.)  three  times  a  day  is  sometimes  used.  Nar- 
cotics should  be  used  with  caution  and  only  when  specially  indicated, 
as  they  may  diminish  the  expectoration  and  favor  stagnation. 

(d)  Postural  Treatment. — This  is  more  promising  and  should  be 
tried  in  all  cases.  Quincke3  recommended  the  inclined  supine  position. 
The  patient  lies  flat  in  bed  with  the  head  turned  to  one  side  to  favor 
expectoration.  The  foot  of  the  bed  is  elevated  20  to  30  cm.  This 
position  is  assumed  for  two  to  three  hours  in  the  early  morning  and 
again  in  the  evening.  It  is  well  at  first  to  have  the  bed  horizontal  in 
order  that  the  patient  may  become  accustomed  to  the  supine  position. 
The  method  is  especially  indicated  in  cases  with  cylindric  and  sac- 
cular ectasies,  opening  freely  into  the  bronchi,  situated  in  the  lower 
lobes  and  without  too  tenacious  or  irritating  a  sputum.  More  rapid 
and  complete  evacuation  of  the  secretion,  the  avoidance  of  stagnation, 
and  a  diminution  in  the  size  of  the  cavities  are  sought  by  the  method. 
Among  others,  Jacobson4  and  Schafer5  have  reported  favorable  results. 
The  latter  refers  to  an  experience  with  15  cases  of  bronchiectasis.    Of 

1  Chaplin,  British  Med.' Jour.,  1895,  p.  1371.         2  British  Med.  Jour.,  1S93,  vol.  i. 
3  Berl.  klin.  Woch.,  1898,  p.  525.  "  Ibid.,  1900,  No.  41. 

5  Deut.  Arch.  f.  klin.  Med.,  1908-09,  vol.  xcv. 


BRONCHIECTASIS  125 

10  in  whom  the  disease  involved  the  lower  lobes,  improvement  was 
observed  in  G.  Of  this  number,  the  sputum  so  far  diminished  in  2 
that  the  patients  would  eough  only  a  few  times  at  the  beginning  of  the 
treatment,  and  were  free  from  cough  the  rest  of  the  day.  The  result 
was  uncertain  in  4  of  the  10  cases.  In  the  remaining  5  cases,  the  dis- 
ease involved  the  right  upper  lobe  (2  cases),  the  middle  and  lower 
lobes  (1  case),  and  the  whole  of  both  lungs  (2  cases).  No  improvement 
was  noted  in  this  group.  A  temporary  increase  in  the  amount  of  sputum 
may  be  noted  during  the  first  week  or  two  of  treatment.  In  favorable 
cases,  this  is  followed  by  a  striking  diminution. 

Partial  inversion,  in  which  the  patient  favors  the  evacuation  by 
leaning  face  downward  over  the  side  of  the  bed,  his  hands  resting  on  the 
floor,  may  also  be  tried  several  times  a  day.  Gerhardt's1  prone  position 
and  manual  compression  of  the  thorax  during  expiration,2  Rossbach's3 
chair,  and  SchreiberV  corset  and  thorax  compressor  may  also  be  used. 
Ewart5  has  devised  an  apparatus  for  children  by  means  of  which 
exercising  may  be  done  in  the  prone  position. 

(e)  Surgery. — This  is  unsatisfactory.  Of  57  operations  collected 
by  Garre,6  21  patients  died  immediately  or  within  the  first  few  weeks 
thereafter.  Forty-six  patients  (80  per  cent.)  were  reported  as  cured, 
but  among  them  unfortunately  little  more  than  a  half  could  be  regarded 
as  actually  cured.  The  remainder  had  fistulse,  chronic  bronchitis  or 
evidence  of  persistent  bronchiectasis.  The  reports  of  individual  opera- 
tors of  large  experience  are  even  less  encouraging.     Thus  Korte7  lost 

11  (73  per  cent.)  of  15  patients  operated  for  bronchiectasis.  Three 
died  immediately  after  operation.  A  fourth  died  seven  hours  after 
operation  and  the  remaining  7  within  three  days  to  three  months. 
Four  patients  (Numbers  10,  24,  36  and  30)  only  were  cured,  and  of 
these  a  successful  result  was  attained  in  3  only  after  repeated 
operations.  One  of  the  3  (No.  30)  was  subjected  to  extensive 
costatectomy,  pneumotomy,  and  final  resection  of  the  right  lower  lobe. 

In  the  consideration  of  surgery,  it  should  be  remembered  that  the 
diagnosis  is  difficult.  The  extent  and  number  of  the  dilatations  cannot 
be  determined  with  certainty.  The  cavities  are  likely  to  be  deep 
within  the  substance  of  the  lung  and  surrounded  by  indurated  tissue, 
thus  increasing  the  danger  of  hemorrhage  and  preventing  the  collapse 
of  the  lung.  Persistent  pulmonary  fistulas  not  infrequently  follow 
operation. 

Disseminated  bilateral  bronchiectasis  and  tuberculous  lesions  are 
not  as  yet  amenable  to  surgery.  With  circumscribed  multiple  or  iso- 
lated saccular  ectasies,  a  resort  to  surgical  interference  may  be  con- 

1  Zeit.  f.  Diat.  u.  physik.  Ther.,  Bd.  i,  p.  11. 

2  Gerhardt,  Berl.  klin.  Woch.,  1873,  No.  23,  p.  25. 

3  Lehrbuch  der  physikal.  Heilmethoden,  2  Aufl.,  S.  59. 
*  Zeit.  f.  klin.  Med.,  Bd.  xiii,  p.  320. 

6  Reports  of  the  Society  for  the  Study  of  Disease  in  Children,  1908,  vol.  iii. 
6  Garre  and  Quincke,  Grundriss  der  Lungenchirurgie,  1903. 
'  Arch.  f.  klin.  Chir.,  1908,  vol.  lxxxv. 


126  DISEASES  OF   THE  BRONCHI 

sidered.  The  outlook  is  in  general  not  sufficiently  favorable  to  advise 
operation  even  in  such  cases,  hut  it  may  be  a  justifiable  procedure 
under  certain  circumstances.  The  disease  may  be  intolerable.  With 
persistent  septic  features,  apparently  due  to  insufficient  drainage  or 
complicating  gangrene,  operation  may  be  undertaken  as  a  life-saving 
measure.  The  operative  technic  is  like  that  for  abscess  or  gangrene. 
Of  the  various  operative  procedures,  pneumectomy  is  a  desperate 
measure.  Extensive  resection  of  the  ribs  overlying  the  pulmonary 
lesions  may  be  followed  by  partial  collapse  of  the  involved  lung  and 
an  amelioration  of  the  symptoms.  Incision  and  drainage  of  a  large 
cavity  may  be  successful.  In  rare  instances,  even  when  the  site  of  the 
disease  is  not  found,  pus  may  later  discharge  into  the  canal.  Several 
operations  may  be  necessary  to  secure  drainage  of  nearby  cavities  into 
the  principal  opening. 

Artificial  Pneumothorax. — This  method  has  been  used  in  the  treat- 
ment of  bronchiectasis  in  a  number  of  instances,  but  without  note- 
worthy success.  The  usual  multiple  character  of  the  lesions  and  the 
frequency  of  extensive  indurative  changes  in  the  lung  diminish  the 
chances  of  a  favorable  result.  A  complicating  adhesive  pleurisy  is  so 
common  as  to  add  greatly  to  the  difficulty  and  danger  of  the  operation. 
The   procedure  cannot  be  recommended. 


CONGENITAL   BRONCHIECTASIS. 

In  rare  instances,  bronchiectasis  is  found  in  the  fetus,  in  dead-born 
children,  or  from  its  anatomic  character  appears  to  be  due  to  per- 
sistence of  a  part  of  the  lung  in  the  fetal  condition.  It  may  exist 
throughout  both  lungs,  or  it  may  be  unilateral  or  unilobar.  Edens1 
has  collected  and  classified  the  reported  cases  to  1904.  Two  principal 
groups  are  described. 

Fetal  Bronchiectasis. — (Congenital  cystic  formation  of  the  lungs; 
congenital  cystic  malformation  of  the  lungs.) — Grawitz2  described  as 
"universal  bronchiectasis"  cases  in  which  the  principal  bronchus 
and  its  main  branches  to  one  lung  or  one  lobe  were  dilated.  There  is 
a  large  central  cyst.  Secondary  and  tertiary  cysts  communicate  with 
this  and  with  each  other.  The  inner  surface  of  the  cysts  is  lined  with 
ciliated  epithelium.  In  a  second  group,  he  termed  the  condition 
"telangiectatic  bronchiectasis."  Here  there  are  numerous  circum- 
scribed ectasies,  developed  from  the  bronchi  of  the  third  and  fourth 
order.  They  may  be  so  placed  that  on  one  branch  several  are  arranged 
one  behind  the  other.  Only  a  small  opening  may  connect  the  bronchus 
and  the  cysts.  In  some  instances,  the  bronchi  end  blindly  and  fail 
to  communicate  with  the  cyst.  Changes  in  the  pulmonary  tissue 
itself  are  generally  lacking.     Cases  of  fetal  bronchiectasis  have  also 

1  Ueber  atelektatische  Bronchiektasie,  Deut.  Arch.  f.  klin.  Med.,  1904,  vol.  lxxxi. 

2  Virchow's  Arch.,  1880,  Bd.  lxxxii. 


CONGENITAL  BRONCHIECTASIS  127 

been  described  by  Meyer,1  Virchow,2  Biermer,3  Barlow,4  Friihwald,5 
Balzer  and  Grandhomme,6  Kaufmann,7  Storck,8  Rokitansky,9  Couve- 
laire,10  Hondo,11  and  Sandoz.12  The  two  cases  reported  by  Sandoz 
were  twin  sisters,  and  he  regarded  the  condition  as  probably  due  to 
congenital  syphilis. 

Atelectatic  Bronchiectasis. — In  this  form,  according  to  Heller,13 
there  has  been  an  arrest  of  development  in  certain  parts  of  the  pul- 
monary parenchyma  (agenesis),  or  well-developed  pulmonary  alveoli 
remain  airless  or  collapse  soon  after  birth.  Gradual  widening  of  the 
bronchi  occurs  in  the  involved  region.  There  are  numerous  multi- 
locular  cavities,  which  may  or  may  not  communicate  with  the  bronchi, 
and  are  lined  with  a  stratified  pavement  epithelium.  Between  the 
dilated  bronchi  are  remnants  of  the  atelectatic  and  non-pigmented 
fetal  lung.  Inflammatory  changes  are  lacking.  The  bronchial  walls 
may  show  an  abnormal  growth  of  cartilage.  Cases  of  this  type  have 
also  been  reported  by  Gairdner.14  Herxheimer,15  Wollman,16  Francke,17 
and  Paul.18 

1  Virchow's  Arch.,  Bd.  xix. 

2  Zur  Entwichelungsgeschichte  des  Kretinismus  und  der  Schadeldifformitat. 

3  Virchow's  Arch.,  1860,  Bd.  xix. 

4  British  Med.  Jour.,  January  3,  1880. 

5  Jahrb.  f.  Kinderh.,  1885,  Bd.  xxiii. 

6  Rev.  mens,  des  mal.  de  l'enfance,  November,  1886. 

7  Untersuchungen  liber  die  sog.  f 6 tale  Rhachitis,  1892. 

8  Wiener  klin.  Woch.,  1897. 

9  Ibid. 

10  Ann.  de  gynec.  et  d'obstet.,  1903. 

11  Zentralb.  f.  allg.  Path.,  February  29,  1904. 

12  Beitr.  z.  path.  Anat.  u.  z.  Allg.  Path.,  1907,  vol.  xli. 

13  Deut.  Arch.  f.  klin.  Med.,  1885,  Bd.  xxxvi,  S.  189. 

14  Glasgow  Path,  and  Clin.  Soc,  1885. 
16  Breslauer  arztl.  Zeit.,  1887,  No.  3.  _ 

16  Inaug.  Diss.,  Freiburg,  1891. 

17  Deut.  Arch.  f.  klin.  Med.,  1894,  Bd.  lii. 

18  Mitthl.  aus.  den  Hamburgischen  Staatskrankenanstalten,  1899. 


CHAPTER  VII. 

BRONCHIAL  BLASTOMYCOSIS. 

Castellani1  has  described  cases  of  bronchitis  with  large  numbers 
of  organisms  resembling  those  described  in  the  section  on  Pulmonary 
Blastomycosis  in  the  Sputum.  In  mild  cases  there  is  mucopurulent 
sputum  without  blood,  and  examination  shows  a  few  coarse  moist 
rales,  or  is  negative.  Recovery  may  take  place  in  the  course  of  several 
weeks  or  months.  In  severe  cases  there  may  be  fever,  emaciation, 
mucopurulent  and  bloody  expectoration.  Signs  of  pulmonary  involve- 
ment may  be  present  on  examination.  In  this  type  the  condition 
may  closely  resemble  phthisis  and  the  outlook  is  grave. 

1  Bronchooiidiosis,  Jour.  Trop.  Med.,  April  1,  1913. 


SECTION   II. 

DISEASES  OF  THE  LUNGS. 


CHAPTER    VIII. 


ATELECTASIS. 

Atelectasis  (from  are/^'c,  incomplete,  and  exraa^,  dilatation)  is 
a  condition  of  the  whole  or  a  part  of  the  lungs  in  which  there  is  a 
persistence  of  or  return  to  a  fetal  and  airless  state. 

Historical  Note. — Atelectasis  in  the  newborn,  previously  regarded 
as  pneumonia,  was  first  described  by  Jorg1  in  1832.  It  was  more 
thoroughly  studied  and  differentiated  from  pulmonary  inflammation 
by  Hasse2  in  1841.  Legendre  and  Bailly3  first  recognized  an  acquired 
form  of  the  disease.  Mendelsohn4  showed  experimentally  that  the 
introduction  of  foreign  bodies  (shot,  paper-ball,  thick  watery  solution 
of  gum  arabic)  into  the  air  passages,  narrowing  of  the  trachea  by  means 
of  a  ligature,  opening  the  pleural  cavity,  or  section  of  both  recurrent 
laryngeal  or  both  vagus  nerves  was  followed  by  atelectasis.  He 
suggested  that  persistence  of  an  open  foramen  ovale,  in  connection 
with  atelectasis,  was  due  to  deficient  respiration,  and  called  attention 
to  the  transition  of  atelectasis  into  pneumonia.  Traube5  showed  that 
the  atelectasis  following  section  of  the  vagus  or  recurrent  laryngeal 
nerves  was  due  to  the  entrance  of  buccal  secretion  into  the  air  passages. 

Classification. — The  term  congenital  atelectasis  is  applied  to  the  con- 
dition when  parts  or  the  whole  of  one  or  both  lungs  persist  in  an 
uninflated,  fetal  state.  The  term  acquired  atelectasis  or  'pulmonary 
collapse  is  used  with  reference  to  cases  in  which  a  previously  air-holding 
lung  returns  to  a  fetal  and  airless  state.  The  acquired  form  of  the 
disease  may  be  due  to  (1)  obstruction  of  the  air  passages  or  to  (2) 
retraction  or  compression  of  the  lung. 

1  De  morbo  pulmonum  organico  ex  respiratione  neonatorum  imperfecta  orto,  Diss. 
Lipsiae,  1832;  and  Die  Fotuslunge  im  geborenen  Kinde  fur  Pathologie,  Therapie  und 
gerichtl.  Arznei-Wissenschaft,  Grimma,  1835. 

2  Spec.  path.  Anat.,  Leipzig,  1841,  p.  324. 

3  Arch.  gen.  de  med.  jour,  complementaire  des  sc.  med.,  1844,  4  ser.,  T.  iv. 

4  Der  Mechanismus  der  Respiration  und  Circulation,  etc.,  Berlin,  1845. 
6Beitr.  z.  exper.  Path.  u.  Phys.,  1846,  Heft  1. 

9 


13U  DISEASES  OF  THE  LUNGS 

Etiology. — Atelectasis  may  occur  at  any  age.  It  is  most  common 
in  the  newborn  as  a  congenital  manifestation.  The  disease  is  more 
frequent  in  infancy  and  early  childhood  than  in  later  years,  probably 
because  of  the  relative  weakness  of  the  respiratory  muscles  at  this 
age  and  the  greater  readiness  with  which  small  air  passages  become 
occluded. 

Congenital  Atelectasis. — This  may  be  due  to  deficient  strength  of  the 
respiratory  muscles,  as  in  premature  or  weakly  infants  or  to  dimin- 
ished irritability  of  the  respiratory  centre  in  consequence  of  intra- 
cranial hemorrhage,  compression  of  the  skull  or  injury  to  the  spinal 
cord  during  birth.  Difficult  or  protracted  labor  favors  its  develop- 
ment. 

Mechanical  obstruction  to  the  entrance  of  air  into  the  lungs 
from  the  inhalation  of  amniotic  fluid,  meconium  or  mucus  before, 
during  or  immediately  after  birth  is  a  more  important  and  more 
frequent  cause. 

Acquired  Atelectasis.— In  some  instances,  the  lungs  are  found  in  a 
fetal  and  airless  condition  in  infants  who  have  come  into  the  world 
alive,  cried  and  lived  several  hours  or  even  days. 

Obstruction  Atelectasis. — Atelectasis  may  be  observed  in  the  course 
of  rickets,  whooping  cough,  croup,  capillary  bronchitis,  measles, 
scarlet  fever,  chronic  diarrhea,  typhoid  fever,  and  acute  rheumatism. 
Occlusion  of  the  bronchi  by  tenacious  secretion  is  probably  the  essen- 
tial cause.  Weakness  of  the  respiratory  muscles  may  be  a  predisposing 
factor.  In  typhoid  fever,  the  development  of  atelectasis  is  favored 
by  insensitiveness  to  ordinary  stimuli,  weakness  of  the  respiratory 
muscles,  ineffectual  efforts  to  expel  bronchial  secretion,  meteorism, 
and  the  maintenance  for  long  periods  of  one  position,  as  lying  on  the 
back. 

Atelectasis  may  also  follow  bronchial  obstruction  by  mucopurulent 
or  fibrinous  secretion,  aspirated  foreign  bodies  or  tumors  growing 
from  the  wall  of  the  bronchus.  Occlusion  of  the  bronchi  by  com- 
pression from  without,  as  from  enlarged  glands  or  new  growths  of  the 
mediastinum,  may  also  be  a  cause.  Complete  occlusion  is  essential 
to  its  production. 

Retraction  or  Compression  Atelectasis. — Atelectasis  may  be  due  to 
encroachment  upon  pulmonary  space  by  the  presence  of  tumors  arising 
from  the  thoracic  structures,  the  chest  wall  or  by  metastasis  from  with- 
out, the  accumulation  of  fluid  or  gas  in  the  pleural  or  pericardial  sac, 
enlargement  of  the  heart,  deviation  of  the  spine  or  elevation  of  the 
diaphragm  (as  from  meteorism,  ascites,  etc.).  The  affected  part  of 
the  lungs  retracts  until  its  elasticity  is  spent.  Actual  compression 
occurs  only  when  a  fully  retracted  lung  is  subjected  to  a  force  which 
still  further  diminishes  its  size. 

Pathogenesis. — The  origin  of  congenital  atelectasis  is  easy  to  under- 
stand and  need  not  be  further  considered.  In  those  cases  in  which 
atelectasis  is  found  in  infants  who  have  cried  and  died  shortly  after 


ATELECTASIS  131 

birth,  at  least  partial  inflation  of  the  lung  may  be  assumed.  In  expla- 
nation of  the  airless  condition  of  the  lungs  in  such  cases,  Thomas1 
suggested  that  slightly  less  air  is  taken  in  during  each  gradually  failing 
inspiration  than  is  expelled  during  expiration.  The  disparity  between 
intake  and  outgo  ends  in  complete  deflation  and  pulmonary  collapse. 
Schroder2  likewise  supported  this  hypothesis.  Disappearance  of  air 
from  that  part  of  the  lung  supplied  by  an  obstructed  bronchus,  in 
Gairdner's3  opinion,  was  due  to  the  peculiar  relation  of  the  obstruction 
to  the  bronchial  wall.  He  suggested  that  a  mucus  plug  may  act  as 
a  ball-valve  in  a  bronchial  tube  of  diminishing  caliber,  allowing  the 
air  to  escape  but  preventing  its  entrance  into  the  involved  pulmonary 
region. 

These  hypotheses,  however,  do  not  serve  to  explain  the  disappearance 
of  air  from  a  part  of  the  lung  excluded  from  communication  with  the 
outside  world  by  a  foreign  body  firmly  fixed  in  a  bronchus.  The  per- 
sistence of  air  in  an  excised  lung  makes  it.unlikely  that  purely  mechan- 
ical factors  are  a  sufficient  explanation.  Virchow  appears  to  have  been 
the  first  to  suggest  that  the  air  was  absorbed  by  the  circulating  blood. 
This  view,  supported  by  Bartels,4  and  by  others  after  him,  was  estab- 
lished as  the  correct  explanation  by  Lichtheim,5  who  showed  that  the 
development  of  atelectasis  in  animals  following  artificial  occlusion 
of  the  bronchus  or  opening  the  pleural  cavity  was  delayed  by  inter- 
ruption of  the  pulmonary  circulation6  at  the  hilus  of  the  lung.  When 
the  lungs  were  inflated  with  oxygen,  carbon  dioxide  or  nitrogen  gas, 
introduced  through  the  trachea,  and  the  left  bronchus  was  tied,  it  was 
found  that  oxygen  and  carbon  dioxide  were  absorbed  more  quickly, 
nitrogen  less  quickly,  than  atmospheric  air.  The  deflation  of  a  lung 
removed  from  the  body  takes  place  more  slowly  than  from  the  lung 
in  a  living  animal  with  an  open  pleural  cavity.  Air  disappears  more 
slowly  from  an  inflated  lung  removed  from  the  body  and  with  the 
bronchus  tied,  than  from  an  inflated  lung  in  the  living  animal  with  the 
bronchus  similarly  tied.  Atelectasis  arising  in  consequence  of  bronchial 
occlusion  or  opening  the  pleural  cavity  may  therefore  be  regarded  as 
due  to  absorption  of  air  by  the  circulating  blood.  Complete  expulsion 
of  air  through  the  bronchi  may  be  prevented  even  when  the  bronchi 
are  patent  by  the  approximation  of  the  bronchial  walls  as  the  lung 
retracts.  Atelectasis  in  connection  with  even  inconsiderable  encroach- 
ment upon  pulmonary  space  is  also  to  be  regarded  as  due  to  absorp- 
tion of  air. 


1  Nederl.  Tijdschr.  vor  Geneesk.,  June,  1864,  viii,  337. 

2  Deut.  Arch.  f.  klin.  Med.,  1869,  Bd.  vi,  p.  398. 

3  Edinburgh  Monthly  Jour.,  1850,  vol.  xii. 

4  Virchow's  Arch.,  vol.  xxi,  S.  132  and  133. 

8  Versuche  iiber  Lungenatelektase,  Arch.  f.  exp.  Path.,  1878-79,  x,  54. 

6  Interruption  of  the  circulation  by  ligating  the  hilus  of  the  lung,  including  the 
bronchus,  the  pulmonary  and  bronchial  arteries  and  the  pulmonary  veins,  gave  incon- 
stant results  owing  to  the  production  of  hemorrhagic  edema,  but  in  isolated  cases  the 
lung  was  completely  airless  throughout, 


132  DISEASES  OF  THE  LUNGS 

Pathology. — The  affected  region  in  congenital  atelectasis  is  uni- 
formly dark  brownish  or  grayish  red,  in  sharp  contrast  with  the  pale 
red  of  the  normal  lung.  It  is  compact,  inelastic,  firm  and  airless.  Con- 
traction is  indicated  by  depression  of  the  involved  area  below  the  level 
of  the  normal  lung.  The  cut  surface  is  smooth,  homogeneous,  non- 
granular and  dry.  Only  a  small  amount  of  blood,  unmixed  with  air, 
can  be  expressed.  The  extent  of  the  process  is  variable  and  may 
embrace  the  whole  of  both  lungs.  Partial  atelectasis,  according  to 
Peiser,1  is  more  likely  to  be  found  in  the  central  parts  of  the  lung,  in 
the  paravertebral  and  suprathoracic  portion.  He  states  that  the  left 
lung  is  more  often  affected  than  the  right.  The  pleura  overlying 
atelectatic  areas  is  at  first  smooth  and  shining,  later  slightly  thick- 
ened and  cloudy.  When  forcible  respiratory  efforts  precede  death, 
subpleural  ecchymoses  may  be  found.  Retraction  of  the  lung  in  con- 
sequence of  atelectasis  may  uncover  the  heart  to  an  abnormal  degree. 
Uninvolved  parts  of  the  lung  may  be  found  in  a  condition  of  acute 
compensatory  inflation. 

Occlusion  atelectasis  is  confined  to  the  region  supplied  by  the 
obstructed  bronchus.  The  areas  are  here  wedge  shaped  with  the  base 
toward  the  periphery  of  the  lung.  Retraction  or  compression  atelec- 
tasis occurs  at  the  site  of  the  encroachment  upon  the  pulmonary 
space.  The  involved  regions  differ  little  in  their  general  characters 
from  the  congenital  form  of  the  disease.  The  color  is,  however,  likely 
to  be  darker  in  consequence  of  circulatory  disturbances,  stasis  and 
pigmentation  of  the  tissue,  and  may  then  be  steel  blue.  Stasis  may 
also  increase  the  amount  of  blood  in  the  tissue  and  more  or  less  dark- 
red  fluid  may  be  expressed  from  the  cut  surface.  Such  an  appearance 
has  been  spoken  of  as  splenization,  and  may  readily  be  confused  with 
hypostatic  pneumonia.  Retraction  or  compression  atelectasis,  in  the 
absence  of  stasis,  may  have  a  gray  or  slaty  color  in  consequence  of  a 
diminished  blood-supply. 

Microscopic  examination  of  congenitally  atelectatic  areas,  according 
to  Peiser,  shows  an  absence  of  alveolar  structure,  rendering  the  pul- 
monary tissue  hardly  recognizable  as  such,  were  it  not  for  the  presence 
of  bronchi.  Beside  the  bronchi  are  cubical  epithelioid  cells  arranged 
in  indistinct  glandular  structure  and  between  them  numerous  blood- 
vessels and  capillaries  filled  with  blood.  Incomplete  atelectasis  shows 
varying  numbers  of  open  alveolar  spaces.  Pulmonary  hemorrhage 
and  edema2  were  frequently  found  to  complicate  the  process. 

Congenitally  atelectatic  areas  can  usually  be  reinflated  when  the 

1  Jahrbuch  f.  Kinderheilk.,  1908,  N.  F.  67,  p.  589. 

2  Peiser's  histological  studies  were  made  after  fixation  of  the  lungs  in  situ  by  means 
of  Gregor's  injection  method:  Before  opening  the  thorax,  the  body  was  injected  by  way 
of  the  inferior  vena  cava  with  one-third  formalin  under  low  pressure  and  the  injection 
continued  as  long  as  foamy  fluid  flowed  from  the  nose  and  mouth.  Ungar  (Zur  Lehre 
von  der  Lungenatelektase,  Jahrbuch  f.  Kinderheilk.,  1909,  N.  F.  69,  p.  505)  criticises 
his  results  and  suggests  that  the  histologic  picture  obtained  was  modified  by  the 
injection.     For  Peiser's  reply  see  ibid.,  p.  673. 


ATELECTASIS  133 

infant  has  died  within  a  few  days  after  birth.  After  a  time,  the  length 
of  which  cannot  be  definitely  stated,  the  affected  regions  in  all  forms 
of  atelectasis  become  incapable  of  redistention.  When  we  consider 
the  unfolding  at  birth  of  the  fetal  lung,  it  seems  improbable  that 
atelectasis  alone  is  responsible.  Inability  of  the  atelectatic  lung  to 
redistend  may  be  due  to  persistence  of  the  cause  of  the  process  or  to 
invasion  of  the  involved  region  with  bacteria  and  consequent  inflam- 
matory changes.  Dunin1  in  his  experimental  study  of  the  pulmonary 
changes  following  the  production  of  exudative  pleurisy  found  that 
the  affected  lung  at  first  showed  degeneration  and  desquamation  of 
the  alveolar  epithelium,  partial  collapse  of  the  capillaries,  and  small- 
celled  infiltration  about  the  larger  bloodvessels  and  the  medium  and 
larger  bronchi,  from  which  in  the  later  stages  fibrous  connective 
tissue  developed.  The  degenerative  process  leads  to  transformation 
of  the  parenchyma  into  connective  tissue  and  obliteration  of  the 
bronchi.  Such  changes  are  doubtless  in  part  responsible  for  the  inability 
of  the  lung  to  re-expand  after  retraction  or  compression  atelectasis. 
Inflammatory  thickening  of  the  pleura  is  also  of  importance  in  this 
form  of  the  disease.  Similar  inflammatory  pulmonary  changes  are 
likely  to  complicate  persistent  types  of  congenital  and  obstruction 
atelectasis  and  render  the  lung  undistensible. 

Early  in  the  course  of  the  atelectasis,  invasion  of  the  involved  parts 
of  the  lung  with  bacteria  which  gain  entrance  through  the  bronchi 
may  lead  to  outspoken  bronchopneumonia.  Hypostatic  pneumonia 
may  also  complicate  the  condition. 

The  final  outcome  of  persistent  atelectasis  was  first  described  by 
Heller2  who  showed  that,  following  the  congenital  form  of  the  disease, 
there  is  in  many  of  the  cases  an  atrophy  of  the  alveoli,  hypertrophy 
of  the  bronchi,  and  the  formation  of  so-called  "atelectatic  bronchiec- 
tasis" in  the  involved  region.  Absence  of  pigment  was  a  striking 
feature  in  adults  with  deeply  pigmented  lungs.  Heller's  findings 
have  in  general  been  confirmed,  among  others  by  Recklinghausen,3 
Herxheimer4  (3  cases),  Berlin,5  Francke,6  Arnheim,7  Paul,8  and  Lot- 
mar9  (2  cases).  Certain  minor  differences  in  the  pathologic  picture 
may  be  noted.  Thus,  absence  of  hyperplasia  of  bronchial  cartilage 
was  noted  by  Herxheimer  (Case  3),  Recklinghausen,  Paul,  and  Lotmar 

1  Anatomische  Veranderungen  in  den  Lungen  bei  deren  Compression,  Virchow's 
Arch.,  1885,  cii,  323. 

2  Die  Schicksale  atelektatischer  Lungenabschnitte,  Deut.  Arch.  f.  klin.  Med.,  1885, 
xxxvi,  189. 

3  Schuchardt,  Inveterierte  Atelektase,  Virchow's  Arch.,  1885,  Bd.  ci. 

4  Beitrage  z.  Kenntniss  atelektatischer  Bronchiektasien,  Bresl.  arztl.  Zeit.,  1887. 
6  Ueber  einen  Fall  von  atelektatischer  Bronchiektasie,  Diss.  Kiel,  1891. 

6  Lungenschrumpfung  aus  der  ersten  Lebenzeit,  Deut.  Arch.  f.  klin.  Med.,  1893,  Bd.  lii. 

7  Ueber  einen  Fall  von  kongenitaler  halbseitiger  Hypertrophic  mit  angeborenen 
Bronchiektasien,  Virchow's  Arch.,  1898,  Bd.  cliv. 

8  Munch,  med.  Woch.,  1899,  S.  30. 

9  Ein  Beitrag  z.  Kenntniss  der  Schicksale  der  fotalen  Atelektase,  Virchow's  Arch., 
1908,  cxci,  28. 


134  DISEASES  OF  THE  LUNGS 

('2  cases.)  Traces  of  pigment  were  found  on  microscopic  examination 
by  Herxheimer  (Case  3),  Francke,  Arnheim,  and  Lotmar  (2  cases). 
Bronchiectasis  was  absent  in  both  of  Lotmar's  cases.  In  one  of  them 
in  which  the  condition  had  lasted  for  fifty  years,  the  alveolar  structure 
of  the  subpleural  parenchyma  was  retained  without  adhesion  of  the 
alveolar  walls. 

Medicolegal  Aspect. — Principal  interest  centres  in  the  importance 
which  can  be  attached  to  air-holding  lung  as  evidence  of  the  birth  of 
a  living  child,  or  to  complete  atelectasis  of  the  newborn  as  evidence 
of  a  dead-born  child. 

The  presence  or  absence  of  air  is  usually  determined  by  testing  the 
lungs  in  water.  If  the  lung  floats,  or  if  on  section  air  escapes,  it  suggests 
that  the  infant  has  lived  and  breathed  after  birth,  but  the  evidence 
cannot  be  regarded  as  conclusive.  Intra-uterine  inflation  of  the  lungs 
may  follow  the  entrance  of  atmospheric  air  into  the  uterus  through 
the  vagina.  Putrefaction  by  gas-forming  bacteria  may  lead  to  the 
presence  of  gas  in  the  lungs  before  or  after  birth.  Artificial  inflation 
of  the  lungs  of  a  dead-born  child  may  also  be  responsible  for  a  positive 
test.  Ahlfeld1  reports  the  presence  of  aspirated  vernix  caseosa,  giving 
an  appearance  of  air-holding  tissue  to  parts  of  the  lung.  In  one  of  his 
cases,  small  pieces  of  the  lung,  although  airless,  floated  in  water. 

On  the  other  hand,  complete  atelectasis  suggests  a  dead-born  child, 
but,  as  already  mentioned,  may  be  found  in  infants  who  have  come  into 
the  world  alive,  lived  several  hours  or  even  days,  and  have  cried. 
Lichtheim's  experiments  make  it  probable,  as  Ungar2  holds,  that  the 
air  may  be  absorbed  from  the  lungs  by  the  blood,  provided  the 
circulation  outlasts  the  respiration. 

Effect  of  Atelectasis  on  the  Circulation. — The  congenital  form  of  the 
disease  is  most  important  owing  to  the  extent  of  pulmonary  involve- 
ment and  the  disturbance  of  the  fetal  circulation.  Jorg  constantly 
found  the  foramen  ovale  open  in  dead-born  infants  with  atelectasis. 
Hasse  confirmed  this,  but  rightly  suggests  that  a  patent  foramen 
ovale  is  not  uncommon  at  this  age.  Weber3  found  the  ductus  arteriosus 
open  in  infants  who  had  breathed  imperfectly.  Atelectasis  excludes 
a  part  of  the  lung  from  the  pulmonary  circulation,  maintains  an 
abnormally  high  pressure  in  the  pulmonary  circuit,  and  thus  tends 
to  continue  the  passage  of  blood  through  these  fetal  channels,  prevent- 
ing their  closure.  In  Francke's  patient,  a  man  aged  fifty-eight  years, 
with  partial  congenital  atelectasis  of  both  lower  lobes,  the  foramen 
ovale  was  found  at  autopsy  to  be  wide  open  and  the  ductus  arteriosus 
was  obliterated.     Stasis  in  the  pulmonary  circuit  leads  also  to  dila- 

1  Schwimmende  Lungen  ohne  Luftgehalt,  Zeit.  f.  Geburtshulfe  und  Gyniikologie, 
1907-08,  lxi,  473. 

2  Konnen  die  Lungen  Neugeborener,  die  geathmet  haben,  wieder  luftleer  werden? 
Vierteljahrschr.  f.  ge.  Med.,  etc.,  N.  F.,  Bd.  xxxix,  H.  1. 

3  Beitrage  z.  path.  Anat.  d.  Neugeb.,  2  Lief,  quoted  from  Strassmann,  Anatomische 
und  physiologische  Untersuchungen  uber  den  Blutkreislauf  beim  Neugebornen,  Arch, 
f.  Gynak.,  1894,  vol.  xlv. 


ATELECTASIS  135 

tation  of  the  right  heart,  and  may  favor  the  formation  of  thrombi  in 
the  right  heart,  the  cerebral  sinuses  or  elsewhere  in  the  venous  system. 

Symptoms. — Congenital  Atelectasis. — In  extreme  cases,  the  infant 
is  asphyxiated  at  birth,  and  efforts  at  resuscitation  fail  or  are  only 
partially  successful.  In  less  severe  cases,  the  infant  may  live  for  a  few 
days  or  even  weeks.  It  is  usually  feeble  and  poorly  nourished,  may 
refuse  to  nurse,  cries  feebly  or  not  at  all,  and  is  dull  and  drowsy.  The 
breathing  is  rapid  and  shallow.  The  cyanosis  is  marked  and  gradually 
increases.  It  is  due  to  encroachment  upon  pulmonary  space,  resulting 
stasis  in  the  venous  system  and  admixture  of  venous  and  arterial  blood 
through  the  persistent  fetal  channels.  The  pulse  is  feeble,  the  extrem- 
ities relaxed  and  cold,  and  the  superficial  veins  dilated.  Cough  and 
fever  are  absent  unless  the  condition  is  complicated.  Toward  the  end 
there  may  be  muscular  twitchings  or  convulsions.  The  child  becomes 
unconscious  and  dies  from  asphyxia  or  exhaustion.  If  the  pulmonary 
involvement  is  slight  and  the  infant  well  nourished  and  strong,  infla- 
tion of  the  unexpanded  lung  may  gradually  take  place.  In  such  cases 
complete  recovery  may  follow.  In  rare  instances,  the  infant  survives 
and  the  atelectasis  persists  as  a  permanent  defect  in  a  part  of  the 
lung.  Small  areas  of  atelectasis  probably  occur  without  producing 
any  symptoms. 

As  described  by  Gerhardt,1  in  cases  in  which  the  atelectasis  is  some- 
what extensive,  the  breathing  is  of  the  stenotic  type  with  inspiratory 
depression  of  the  intercostal  spaces,  the  clavicular  fossae  and  the 
neighborhood  of  the  sixth  and  seventh  chondral  cartilage,  where  a 
transverse  furrow,  in  part  due  to  the  tug  of  the  diaphragm,  may  be 
seen. 

Physical  signs,  when  present,  are  like  those  in  pneumonia,  with 
which  the  disease  was  formerly  confused.  The  percussion  note  is  dull 
or  dull  and  tympanitic.  The  dulness  is  seldom  marked  and  may  be 
difficult  of  determination,  when,  as  is  commonly  the  case,  the  process 
is  bilateral.  Gerhardt  states  that  at  first  the  extent,  intensity,  and 
even  the  side  affected  may  be  varied  by  changing  the  position  of  the 
patient.  The  breathing  over  small  areas  is  diminished  and  vesicular. 
When  large  areas  are  involved,  it  may  be  bronchial.  Consonating 
rales  may  also  be  heard.  An  increase  in  vocal  fremitus  may  be  estab- 
lished over  large  areas.  If  the  bronchi  are  plugged,  the  signs  may  be 
those  of  massive  pneumonia,  dulness,  diminished  or  absent  breathing 
and  vocal  fremitus.  The  area  of  cardiac  dulness  may  be  increased 
in  consequence  of  retraction  of  neighboring  parts  of  the  lung  or  dila- 
tation of  the  right  side  of  the  heart.  If  the  stasis  is  extreme,  the  second 
pulmonic  sound  may  be  increased  and  edema  may  be  present. 

In  Francke's  case,  a  man  aged  fifty-eight  years,  in  whom  at  autopsy 
partial  congenital  atelectasis  of  both  lower  lobes  was  found,  there  was 
a  striking  deformity  of  the  chest.    The  thorax  was  lengthened.    The 

1  Handbuch  der  Kinderkrankheiten,  1878,  Bd.  iii,  Halfte  3,  p.  504. 


136 


DISEASES  OF  THE  LUNGS 


anteroposterior  diameter  of  its  upper  portion  was  increased.     The 

upper  part  of  the  sternum  and  the  first  three  ribs  were  bowed  outward, 

the  region  below  the  sixth  rib  was  constricted  (wasp-waist),  and  still 

lower  the  thoracic  margin  was  bent  outward.    In  this  case,  as  in  others 

in  which  the  remote  consequences  of  congenital  atelectasis  have  been 

described,  there  was  chronic  interstitial  pneumonia,  bronchiectasis  and 

emphysema. 

Fig.  21 


'Collapse  induration"  of  the  right  apex.      (Kronig.) 


Acquired  Atelectasis. — In  cases  in  which  the  condition  complicates 
bronchial  or  pulmonary  infection  and  is  due  to  obstruction  of  the 
bronchi  by  tenacious  secretion,  there  are  usually  no  clinical  features 
which  can  with  certainty  be  ascribed  to  atelectasis.  The  symptoms 
and  physical  signs  are  then  commonly  masked  by  the  underlying 
disease.  The  pulmonary  collapse  may  contribute,  however,  to  the 
respiratory  disturbance.  In  some  cases  it  may  be  demonstrated  when 
over  circumscribed  areas,  usually  at  the  bases  posteriorly,  such  signs 
as  dulness,  diminished  or  absent  breathing,  voice,  whisper  and  tactile 
fremitus  partially  or  wholly  disappear  after  cough  and  the  relief  of  the 
obstruction,  on  urging  the  patient  to  breathe  deeply  or  on  changing 
his  position.     Rales  may  be  heard  after  the  obstruction  is  relieved. 


ATELECTASIS  137 

In  mild  cases,  rales  which  disappear  during  the  course  of  the  examina- 
tion may  be  the  only  manifestation. 

When  large  portions  of  the  lung  are  rendered  atelectatic  by  the 
occlusion  of  one  of  the  larger  bronchi,  as  by  an  impacted  foreign  body, 
the  symptoms  and  signs  are  marked.  The  dyspnea  is  likely  to  be 
intense.  Respiratory  motion  and  the  breath  sounds  are  diminished 
or  abolished  over  the  affected  region,  with  dulness,  diminished  or 
absent  voice,  whisper  and  tactile  fremitus.  Inflammatory  processes 
soon  develop  in  the  collapsed  lung  unless  the  obstruction  is  relieved. 

Pulmonary  collapse  in  consequence  of  encroachment  upon  pulmonary 
space,  as  from  a  pleural  effusion,  is  in  part  responsible  for  the  dyspnea 
which  occurs.  The  physical  signs  vary  with  the  extent  of  the  pul- 
monary collapse.  If  this  is  slight,  transient  rales  only  may  be  heard. 
If  the  lung  is  considerably  reduced  in  size,  there  is  likely  to  be  dulness 
or  dull  tympany,  diminished  and  bronchial  breathing  at  times  of  an 
amphoric  quality,,  increased  voice,  whisper  and  tactile  fremitus. 
Consonating  rales  may  also  be  heard.  The  signs  vary  with  the  condi- 
tion of  the  pleura.  X-ray  examination  shows  an  increased  density 
to  the  shadow  over  the  atelectatic  compared  with  the  normal  lung. 

Abrams1  has  called  attention  to  circumscribed  areas  of  atelectasis 
in  apparently  normal  individuals  in  certain  parts  of  the  chest  as  at 
the  margin  of  the  lungs  near  the  inner  and  outer  ends  of  the  clavicles 
anteriorly  and  at  the  outer  border  of  the  lung  in  the  supraspinous  fossa 
and  at  the  angle  of  the  scapula  posteriorly.  These  physiologic  areas 
are  dull  on  percussion.  They  disappear  after  repeated  forced  inspira- 
tions and  reappear  in  a  few  moments  when  tranquil  breathing  is  resumed. 

Kronig2  has  noted  the  presence  of  non-tuberculous  "collapse  indura- 
tion" of  the  right  apex  in  patients  with  obstructed  nasal  breathing. 
The  nasal  obstruction  is  usually  due  to  adenoids  in  the  nasopharynx 
with  which  thickening  of  the  posterior  ends  of  the  turbinates  may  be 
associated.  There  is  retraction  and  diminished  motion  of  the  right 
apex,  dulness  of  varying  degree  over  the  right  supraclavicular  or  supra- 
spinous fossae,  at  times  narrowing  of  the  isthmus,  and  indeterminate 
or  intense  bronchovesicular  breathing.  In  some  cases,  rales  may  also 
be  heard.  General  signs  of  tuberculosis  are  lacking.  Special  stress 
in  excluding  it  is  laid  on  a  normal  respiratory  excursion  of  the  inferior 
pulmonary  margin.  The  apical  collapse  is  ascribed  to  relatively 
greater  inspiratory  expansion  and  diminished  expiratory  collapse  of 
these  compared  with  other  parts  of  the  lungs.  Mouth  breathing 
favors  the  inhalation  of  dust  which  is  deposited  in  largest  amount  at 
the  apices.  Of  the  two,  the  right  is  principally  affected  because  of  the 
greater  diameter  of  the  right  compared  with  the  left  primary  bronchus 
and  the  proportionally  greater  bronchial  and  less  pulmonary  space 
at  the  right  than  at  the  left  apex.     Repeated  catarrhal  swelling  of 

1  Medical  Record,  September  1,  1894. 

2  Ueber  einfache,  nichttuberkulose  Kollapsinduration  der  rechten  Lungenspitze  bei 
chronisch  behinderter  Nasenatmung,  Medizinische  Klinik,  6  Okt.,  1907,  No.  40. 


138  DISEASES  OF  THE  LUNGS 

the  apical  mucous  membrane  is  followed  by  collapse  of  the  involved 
alveolar  region,  with  subsequent  chronic  inflammatory  thickening, 
fibrous  induration,  and  contraction. 

Diagnosis. — This  is  not  difficult  in  the  congenital  form  of  the  dis- 
ease. The  occurrence  of  the  pulmonary  symptoms  at  or  soon  after 
birth,  the  cyanosis,  absence  of  cough  and  fever,  and  the  bilateral  site 
of  the  process  usually  serve  to  exclude  pneumonia.  Congenital  atelec- 
tasis as  a  cause  of  pulmonary  changes  in  adult  life  can  hardly  be  recog- 
nized before  an  autopsy  is  performed.  In  the  acquired  form  secondary 
to  bronchial  occlusion,  change  in  the  signs  on  shifting  the  position  of 
the  patient  or  after  cough  and  deep  breathing  is  suggestive  evidence 
against  edema  or  pneumonia  developing  at  the  bases.  Atelectasis  is 
an  adequate  explanation  for  rales  or  signs  of  consolidation  in  the  im- 
mediate neighborhood  of  an  encroachment  upon  pulmonary  space. 
Disappearance  of  the  signs  after  removal  of  the  cause  may  be  necessary 
to  exclude  a  complicating  pulmonary  process.  Transient  rales  at  the 
margin  of  the  lungs,  especially  in  the  axillary  region,  in  the  absence  of 
other  symptoms  or  signs  of  pulmonary  disturbance  may  be  regarded 
as  physiologic. 

Prognosis. — The  outlook  in  congenital  atelectasis  depends  on  the 
extent  of  the  process,  the  nutrition  and  strength  of  the  infant.  The 
prognosis  of  the  acquired  form  is  that  of  the  cause  of  the  disease. 

Treatment. — The  treatment  of  congenital  atelectasis  is  that  of 
asphyxia.  Aspirated  fluids  and  mucus  must  be  wiped  from  the  nose 
and  mouth,  and,  if  necessary,  aspirated  from  the  trachea  by  means  of 
a  catheter.  The  respiration  should  be  stimulated  by  slapping  and 
rubbing  the  body,  alternate  immersion  in  hot  and  cold  water,  and,  if 
need  be,  by  artificial  means.  Sylvester's1  method  should  be  used, 
the  infant  meanwhile  lying  on  its  back,  warmly  covered,  with  the  feet 
fixed  and  the  tongue  drawn  forward  to  prevent  obstruction  of  the  air 
passages.  The  arms,  grasped  just  above  the  elbows,  are  then  alter- 
nately raised  above  the  infant's  head  and  lowered  to  the  sides  of  the 
chest  against  which  they  are  pressed.  Schultze's  swinging  movements 
may  also  be  used.  If  these  measures  fail,  insufflation  by  means  of  a 
catheter  introduced  into  the  trachea  may  be  tried,  care  being  taken, 
however,  to  avoid  forcible  inflation  for  fear  of  producing  vesicular 
and  interstitial  emphysema.  After  successful  resuscitation,  special 
attention  should  be  paid  to  maintaining  the  body  temperature.  The 
child  may  be  rolled  in  cotton  and  surrounded  by  hot-water  bottles 
or  placed  in  an  incubator.  Care  should  be  taken  not  to  constrict  the 
chest  by  tight  application  of  clothing.  Persistence  of  partial  atelec- 
tasis or  recurrence  should  be  treated  by  daily  repetition  of  slapping, 
friction,  and  bathing,  by  inducing  the  infant  to  cry  and  by  frequent 
changes  of  position.  Careful  attention  should  be  paid  to  appropriate 
feeding. 

1  The  True  Physiological  Method  of  Restoring  Persons  Apparently  Drowned  or  Dead 
and  of  Resuscitating  Stillborn  Children,  London,  1858. 


ATELECTASIS  139 

The  treatment  of  acquired  atelectasis  is  that  of  the  cause  of  the 
disease.  In  the  obstructive  form,  due  to  retention  of  secretion,  the 
general  strength  should  be  maintained  by  proper  attention  to  food  and 
fresh  air,  thus  favoring  the  expulsion  of  bronchial  secretion.  An 
expectorant  may  also  be  of  service.  Frequent  changes  in  position  of 
a  patient  lying  in  bed  favor  the  relief  of  the  obstruction.  In  typhoid 
fever,  cool  baths,  frequent  changes  of  position,  and  the  relief  of  meteor- 
ism  are  important  measures.  Aspirated  foreign  bodies  should  be 
removed.  Secondary  inflammatory  changes  are  likely  to  permanently 
impair  the  collapsed  lung  if  the  obstruction  is  allowed  to  remain  more 
than  a  few  days.  The  early  removal  of  pleural  effusion  may  prevent 
the  development  in  and  about  the  collapsed  lung  of  inflammatory 
changes  which  render  it  undistensible. 


CHAPTER  IX. 

EMPHYSEMA. 

Classification. — The  term  Emphysema  (from  E/j^uarjiia  an  infla- 
tion) when  used  without  qualification  usually  indicates  what  may 
more  specifically  be  spoken  of  as  Diffuse  Vesicular  Emphysema.  It 
is  to  be  distinguished  from  other  forms  which  differ  sufficiently  to 
warrant  their  consideration  under  separate  divisions,  as  Acute  Vesicular 
E.,  Compensatory  E.,  Senile  E.,  and  Interstitial  E. 

1.  DIFFUSE   VESICULAR   EMPHYSEMA. 

Definition. — Diffuse  vesicular  emphysema,  also  known  as  Ordinary, 
Genuine  or  True  E.,  Hypertrophic  E.,  Large-lunged  E.,  Substantive  or 
Idiopathic  E.,  is  a  chronic  condition  in  which  the  infundibular  passages 
and  the  alveoli  are  dilated  and  the  alveolar  walls  atrophied  more  or 
less  generally  throughout  the  lungs.  It  is  characterized  clinically  by 
varying  degrees  of  dyspnea  and  cyanosis. 

Etiology. — The  condition  is  almost  invariably  associated  with  other 
pathologic  bronchial  or  pulmonary  changes  accompanied  by  cough. 
It  is  a  mistake  to  regard  emphysema  as  idiopathic  or  essential.  It  is 
usually  secondary  to  bronchial  or  bronchopulmonary  disturbances. 
Chronic  bronchitis  in  connection  with  bronchopulmonary  infection 
or  cardiac  insufficiency,  with  a  harassing  dry  cough  and  tenacious, 
mucoid  secretion  is  the  most  frequent  cause.  Next  in  importance  is 
bronchial  asthma.  Whooping  cough  is  an  occasional  cause.  In  rare 
instances  it  is  said  that  emphysema  may  follow  partial  obstruction 
of  the  larger  air  passages,  as  from  nasal,  pharyngeal,  laryngeal  or 
tracheal  obstruction.  Compression  of  the  trachea  from  without,  as 
by  goitre  or  mediastinal  new  growths,  is  said  to  also  be  a  cause. 

Certain  occupations  have  been  said  to  predispose  to  the  condition. 
Thus  players  on  wind  instruments,  glass-blowers,  singers,  and  laborers 
who  lift  heavy  weights  have  been  regarded  as  subject  to  the  disease. 
Straining  at  stool  is  also  mentioned  as  a  possible  cause.  Forlanini1 
could  determine  no  difference  in  the  vital  capacity,  respiratory  pressure, 
or  amplitude  of  the  pulmonary  excursion  among  the  trumpeters  of 
the  Italian  mountain  troops  and  musicians  and  other  bodies  of  men 
among  the  troops  stationed  in  the  level  country.    Fischer2  discovered 

1  Cent.  f.  klin.  Med.,  1891,  No.  17,  p.  310. 

2  Munch,  med.  Woch.,  1902,  No.  17. 


DIFFUSE  VESICULAR  EMPHYSEMA  141 

no  outspoken  case  of  emphysema  among  about  500  military  musicians. 
Prettin  and  Leibkind1  investigated  230  glass-blowers.  Among  164 
occupied  at  the  trade  up  to  forty  years,  no  cases  of  emphysema  were 
found.  Among  54  at  work  from  forty  to  fifty  years,  2  were  found 
to  have  a  slight  degree  of  emphysema,  while  among  12  at  work  over 
fifty  years,  3  showed  the  clinical  picture  of  emphysema  with  much 
diminished  thoracic  excursion  (2  to  4  cm.),  very  slight  diaphragmatic 
motion,  and  diminished  vital  capacity  (2500  to  2700).  They  con- 
clude that  glass-blowing  is  of  no  moment  in  the  etiology  of  emphy- 
sema. 

Among  196,549  out-patient  cases  at  the  Massachusetts  General 
Hospital  from  1905  to  1914  were  557  cases  (0.28  per  cent.)  of 
emphysema.  Of  528  adults,  347  were  males,  181  females.  This 
greater  frequency  among  males  is  common  to  all  statistics  on  the  dis- 
ease, and  may  be  ascribed  to  the  more  frequent  occurrence  among 
men  of  those  diseases  most  likely  to  lead  to  emphysema,  especially 
bronchitis.  The  condition  is  not  commonly  found  before  the  third 
decade  and  becomes  more  frequent  as  age  advances.  Cases  observed 
in  persons  over  sixty-five  to  seventy  are  perhaps  to  be  classed  as  senile 
emphysema. 

In  autopsy  material,  Virchow2  found  emphysema  at  the  Berlin 
Pathological  Institute  during  an  interval  of  nine  years  in  only  0.6 
to  0.7  per  cent,  of  all  cases.  Frankel's3  pathologic  studies  have  the 
merit  of  special  attention  to  the  presence  of  emphysema.  Among 
911  autopsies  performed  from  April  1,  1896,  to  March  31,  1897,  not 
less  than  65  (or  about  7  per  cent.)  showed  extensive  emphysematous 
changes  as  the  essential  condition  of  the  lungs,  associated  only  with 
diffuse  chronic  bronchitis  with  and  without  bronchiectasis.  Of  the  65 
cases,  14  were  from  thirty-one  to  fifty,  34  from  fifty-one  to  seventy. 
Of  the  remaining  17  cases,  15  were  from  seventy-one  to  ninety  and  the 
age  of  two  was  unknown.  The  disparity  between  the  frequency  of 
the  condition  among  clinical  and  autopsy  cases  may  be  ascribed  to  the 
readiness  with  which  the  less  marked  degrees  of  emphysema  may  be 
overlooked  in  the  former. 

Inheritance. — Jackson4  found  that  among  28  patients  with  emphy- 
sema, 18  were  born  of  parents  suffering  from  the  same  disease,  and  in 
some  instances  the  brothers  and  sisters  were  likewise  affected.  On  the 
contrary,  of  50  non-emphysematous  persons,  only  3  had  parents  with 
emphysema.  Lebert5  could  trace  an  inheritance  to  the  disease  in  13 
of  108  cases.  Hertz6  refers  to  one  family,  all  the  members  of  which 
were  affected  with  varying  degrees  of  emphysema. 


1  Munch,  med.  Woch.,  February  5,  1904. 

2  Emphysema  Pulmonum,  Berl.  klin.  Woch.,  1888,  No.  1. 

3  Spez.  Path.  u.  Ther.  der  Lungenkrankheiten,  1904,  p.  219. 

4  Waters,  British  Med.  Jour.,  1860,  p.  1012. 

6  Klinik  der  Brustkrankheiten,  Tubingen,  1874,  p.  394. 

6  Lungenemphysem,  Ziemssen's  Handbuch  der  spec.  Path.  u.  Ther.,  5,  ii,  p.  346. 


142  DISEASES  OF  THE  LUNGS 

Pathogenesis. — In  explanation  of  the  origin  of  emphysema,  two 
principal  theories  are  held,  i.  e.,  the  nutritive  and  the  mechanical  theory. 

Nutritive  disturbances,  singly  or  in  combination  with  mechanical 
factors,  are  regarded  as  an  essential  condition  by  various  authors. 
Thus  Villemin1  referred  emphysema  to  primary  changes  in  the  con- 
nective tissue.  J.  Lange2  assumed  a  paralytic  neurosis  of  the  nerve 
branches  supplying  the  finest  bronchi  and  their  muscle  fibers.  Bayer8 
regarded  changes  in  the  circulation  and  Isaaksohn4  degeneration  of  the 
capillaries  as  the  cause.  Grawitz5  implicates  the  circulation  in  the 
origin  of  emphysema  and  makes  a  division  into  hydropic,  inflammatory, 
and  atrophic  emphysema.  To  Virchow6  an  onset  in  early  youth  was 
suggested  by  the  deficient  pigmentation  of  the  emphysematous  lung, 
and  led  him  to  assume  that  a  primary  disease,  diminishing  the  pul- 
monary elasticity,  was  the  predisposing  cause,  although  mechanical 
factors  may  still  be  of  moment  in  its  further  development.  Eppinger7 
described  a  separation  and  reduction  in  size  of  the  larger  and  disap- 
pearance of  the  smaller  elastic  fibers  in  the  emphysematous  lung. 
He  also  noted  a  laceration  and  splitting  of  the  fibers  with  the  formation 
of  minute  clefts  in  the  alveolar  walls.  Hansemann's8  discovery  of  the 
presence  of  normal  pores  between  the  alveoli  may  in  part  account 
for  apparent  dehiscence  of  the  fibers.  Artefarcts  may  be  responsible 
for  others.  Sudzuki9,  Spalteholtz,10  and  Tendeloo11  failed  to  find  the 
elastic  tissue  altered  to  any  considerable  degree.  Separation  and  reduc- 
tion in  size  of  the  elastic  fibers  may  be  ascribed  to  distention  of  the 
alveoli  in  the  emphysematous  lung. 

Freund12  has  long  held  the  view  (as  his  list  of  publications  shows) 

1  Arch.  gen.  de  med.,  October  and  November,  1866. 

2  Ueber  d.  substant.  Lungenemphysem.  und  dessen  Behandlung  mit  comprimirten 
Luft,  Dresden,  1870. 

3  Arch,  der  Heilkunde,  11  Jahrg.,  1870.  4  Virchow's  Arch.,  vol.  liii. 
6  Deut.  med.  Woch.,  1892,  No.  10. 

6  Verhandl.  d.  Berl.  med.  Gesellschaft.,  1888,  Bd.  xviii. 

7  Prager  Vierteljahrschr.,  1876,  vol.  exxxii. 

8  Ueber  die  Poren  der  normalen  Lungenalveolen.  Sitzungsbericht  der  Konigl.  Preuss. 
Akad.  der  Wissenschaften,  1896,  vol.  xliv. 

'  Virchow's  Arch.,  clvii,  438. 

10  Quoted  from  Hoffman,  Nothnagel,  1902,  American  edition. 

11  Studien  iiber  die  Ursachen  der  Lungenkrankheiten,  Wiesbaden,  1902. 

12  Beitrage  z.  Histologie  d.  Rippenknorpel  im  normalen  und  pathologischen  Zustand., 
Breslau,  1858;  Der  Zusammenhang  gewisser  Lungenkrankheiten  mit  primaren  Rippen- 
knorpelanomalien,  Erlangen.,  1859;  Thorax-anomalien  als  Predisposition  zur  Lungen- 
phthise  und  Emphysem.,  Berl.  klin.  Woch.,  1901;  Die  Beziehung  der  Heilungsvorgangc 
gewisser  Formen  der  Lungenphthise  zur  Gelenkbildung  am  ersten  Rippenringe,  Thera- 
peutische  Monatshefte,  Juni,  1902;  Ueber  primare  Thoraxanomalien  speziell  iiber  die 
starre  Dilatation  des  Thorax  als  Ursache  eines  Lungenemphysems,  Berlin,  1906,  S. 
Kaiser;  Zur  operativen  Behandlung  gewisser  Lungenkrankheiten  insbesondere  auf 
starrer  Thoraxdilatation  beruhenden  alveolaren  Emphysems  (mit  einem  Operations- 
falle),  Zeit.  f.  exp.  Path.  u.  Ther.,  1906,  Bd.  hi,  p.  479;  Beitrage  z.  Behandlung  des 
tuberkulosen  Lungenspitzenphthise  und  des  alveolaren  Emphysems  durch  operative 
Mobilisation  und  des  starr  dilatierten  Thorax,  Munch,  med.  Woch.,  1907,  No.  48; 
Freund  and  Mendelsohn,  Der  Zusammenhang  des  Infantilismus  des  Thorax  und  des 
Beckens,  Stuttgart,  Enke,  1908;  Die  chir.  Behandlung  d.  Stenose  u.  d.  starr.  Dilat. 
d.  Thorax.,  Deut.  med.  Woch.,  1910,  xxxvi,  730;  Ueber  Wechselbeziehungen  zwischen 
Lunge  u.  Thorax  beim  Emphysem.,  ibid.,  1911,  xxxvii,  1254;  Ueber  das  Emphysem. 
Kritik  d.  Arbeit  von  I.  Plesch.,  ibid.,  1913,  xxxix,  19. 


DIFFUSE  VESICULAR  EMPHYSEMA  143 

that  nutritive  changes  in  the  costal  cartilages  followed  by  fibrous  and 
fatty  degeneration,  cavity  formation  and  calcification  lead  to  loss  of 
elasticity,  thickening  and  enlargement,  and  give  rise  to  rigid  thoracic- 
dilatation  and  the  maintenance  of  a  persistent  inspiratory  position. 
He  regards  emphysema  as  a  consequence  of  this  dilatation.  In  a 
considerable  proportion  of  the  cases  of  emphysema  the  costal  carti- 
lages are  thus  changed.  Freund  finds  also  that  in  ordinary  substantive 
emphysema  the  lungs  collapse  on  opening  the  thorax,  thus  suggesting 
that  pulmonary  is  secondary  to  thoracic  dilatation. 

The  objection  may,  however,  be  raised  concerning  these  histologic 
and  anatomic  features  that  they  may  as  reasonably  be  regarded  as  the 
result,  as  the  cause  of  emphysema,  and  that  their  bearing  on  the  etiology 
of  the  disease  is  thus  questionable.  A  predisposition  to  the  disease 
from  congenital  weakness  of  the  pulmonary  tissue  can  neither  be 
denied  nor  affirmed.  In  spite  of  the  difficulty  of  establishing  evi- 
dence in  support  of  nutritive  factors  as  a  cause  of  emphysema,  such 
changes  can  by  no  means  be  wholly  disregarded.  Mechanical  forces 
alone  seem  incapable  in  many  cases  of  producing  emphysema,  as,  for 
example,  in  those  who  play  upon  wind  instruments  or  who  make 
violent  respiratory  efforts  in  their  occupation.  If  mechanical  forces 
alone  were  a  sufficient  cause,  emphysema  would  be  far  more  common 
than  is  actually  the  case.  It  is  therefore  reasonable  to  assume  that 
some  nutritive  disturbance,  whether  congenital  or  acquired,  is  a  prob- 
able predisposing  factor  in  the  development  of  emphysema. 

Mechanical  factors  are  present  in  practically  all  cases.  The  relative 
importance  of  inspiration  and  expiration  has  been  much  discussed. 
Inspiratory  overdistention  of  the  lung  may  occur  in  consequence  of 
exclusion  of  a  part  of  the  lung  from  participation  in  respiratory  motion. 
Compensatory  dilatation  in  alveoli  adjacent  to  areas  of  atelectasis 
may  possibly  be  explained  in  this  way,  but  it  is  difficult  to  exclude  the 
influence  of  nutritive  disturbances  and  heightened  expiratory  pressure 
from  cough  as  factors  of  equal  or  greater  importance.  According 
to  Tendeloo,  emphysema  of  a  purely  inspiratory  type  should  manifest 
itself  in  the  sternoparasternal  and  lateral  caudal  parts  of  the  lung. 
It  is  possible  that  the  pulmonary  dilatation  demonstrated  by  Hof- 
bauer,1  Seefeldt,2  and  Brims3  in  normal  individuals  after  deep  breath- 
ing, in  dyspnea,  air-hunger,  physical  exertion  and  cardiac  insufficiency 
may  have  a  bearing  on  this  question  of  the  mechanical  forces  of  respi- 
ration. In  these  conditions  inspiration  is  more  strongly  increased  than 
expiration,  the  disproportion  being  of  such  a  degree  that  a  part  of  the 
inhaled  air  remains  in  the  lungs,  causing  overdistention.  It  is  con- 
ceivable that  the  persistence  of  respiratory  overexertion  may  induce 
emphysema. 

1  Zur  Emphysemafrage,  Berl.  klin.  Woch.,  21  Marz,  1910,  No.  12. 

2  Der  Stand  des  Zwerchfelles  bei  Gesunden  und  Emphysematiker,  Beitr.  z.  Klin. 
d.  Tuberkul.,  1910,  xv,  457. 

3  Berl.  klin.  Woch.,  7  Feb.,  1910. 


144  DISEASES  OF  THE  LUNGS 

The  expiratory  theory  is  a  more  reasonable  explanation.  During 
forced  expiration  against  the  closed  glottis,  as  in  violent  attacks  of 
cough,  the  thoracic  walls  are  firmly  fixed  and  the  abdominal  contents 
forced  upward  by  contraction  of  the  abdominal  muscles.  The  inferior 
portions  of  the  lungs  are  compressed  and  the  increased  intrapulmonary 
pressure  inflates  the  least  protected  and  more  yielding  cranial  supra- 
thoracic  and  sternoparasternal  regions.  The  emphysema  is  usually 
most  advanced  at  the  apices  and  the  anterior  pulmonary  margins, 
thus  emphasizing  the  importance  of  expiration  in  its  production. 
Repeated  overdistention  may  be  assumed  finally  to  lead  to  diminished 
elasticity  and  permanent  distention. 

Experiments  on  animals  show  that  an  acute  pulmonary  distention 
can  be  mechanically  induced.  In  LichtheimV  experiments,  an  acute 
pulmonary  dilatation  followed  obstruction  of  a  primary  bronchus. 
Ligature  of  the  trachea  by  Hirtz,2  Kohler,3  and  Sudzuki4  produced 
emphysema,  but  stasis  of  bronchial  secretions  may  have  influenced 
the  result.  Expiratory  obstruction  by  means  of  inserted  valves  by 
Marey,5  Cohnheim,6  and  Bert7  led  to  an  acute  pulmonary  distention. 
Schalls  experimented  on  dogs  with  masks  so  constructed  that  inspira- 
tion or  expiration  or  both  could  be  obstructed  at  will.  Inspiratory 
obstruction  for  nine  months  in  one  animal,  expiratory  obstruction  for 
ten  and  one-half  months  in  a  second  and  both  inspiratory  and  expiratory 
obstruction  for  eleven  months  in  a  third  failed  to  produce  emphysema 
or  lead  to  atrophy  of  the  pulmonary  tissue.  Schall  concludes  that 
one  must  be  cautious  in  accepting  the  origin  of  chronic  emphysema 
from  acute  inflation,  and  regards  it  as  probable  that  bronchitis  or 
pneumonia  must  first  injure  the  tissue  before  changes  in  the  respiratory 
mechanism  can  give  rise  to  atrophy  of  the  tissue. 

In  conclusion  it  may  be  stated  as  an  hypothesis  that  emphysema 
arises  when  pulmonary  tissue,  the  nutrition  of  which  is  impaired,  is 
subjected  to  repeated  or  persistent  distention,  whether  by  inspiration 
or  expiration  or  both. 

Pathology. — The  thorax  is  enlarged  in  all  dimensions,  especially  in 
the  anteroposterior  diameter,  and  is  of  a  barrel  shape.  In  a  consider- 
able proportion  of  the  cases  the  costal  cartilages  are  enlarged,  firm, 
inelastic,  and  calcified.  According  to  V.  Salis,9  the  costovertebral 
articulations  show  all  grades  of  transition  from  mild  fatty  degeneration 
to  complete  ossifying  arthritis.  Such  changes  are  present  with  and 
without  emphysema,   increase  in  frequency   as  age  advances,   and 

1  Versuche  iiber  Lungenatelektase,  Arch.  f.  exp.  Path.,  1878-79,  x,  54. 

2  These  de  Paris,  1878. 

3  Arch.  f.  exp.  Path.  u.  Pharmakologie,  Bd.  vii,  p.  1. 

4  Virchow's  Arch.,  1900,  Bd.  xlvii. 

5  Journal  de  l'anatomie  et  de  la  physiologie,  1865,  p.  425. 

6  Vorlesungen  iiber  allg.  Path.,  Berlin,  1882,  ii,  169. 

7  Lecons  sur  la  physiol.  comparee  de  la  respiration,  Paris,  1870. 

8  Beitr.'  z.  Klinik  der  Tuberkulose,  1909,  xiv,  407. 

9  Zur  Bedeutung  der  Rippengelenke  bei  Lungenemphysem  und  Lungentuberkulose, 
Inaug.  Diss.,  Wiesbaden,  1910. 


DIFFUSE  VESICULAR  EMPHYSEMA  145 

appear  to  bear  no  direct  relation  with  the  disease.  Schenker1  finds 
atrophy  of  the  intercostal  muscles  with  and  without  degeneration 
constantly  in  the  severe  forms  of  emphysema,  inconstantly  in  the  less 
severe  but  still  outspoken  forms  and  absent  in  the  mild  cases. 

On  removing  the  sternum,  the  lungs  do  not  collapse  as  usual,  owing 
to  diminished  elasticity.  The  pleura  is  free  or  adherent  if  the  condi- 
tion is  complicated.  The  pulmonary  margins  are  rounded,  cover  the 
pericardium  to  an  abnormal  degree,  and  encroach  upon  the  medias- 
tinum over  which  they  may  meet  or  overlap  in  the  middle  line.  The 
upper  boundaries  extend  abnormally  high  above  the  clavicles  and  below, 
the  lungs  depress  the  diaphragm  to  a  distance  of  one  to  two  costal 
spaces  beyond  the  usual  limit.  The  lungs  may  show  the  impressions 
of  the  ribs  and  pit  readily  on  pressure.  On  palpation,  they  present  a 
peculiar  soft,  feathery  feeling  and  crepitate  but  little  on  pinching. 
On  section,  the  tissue  is  pale,  grayish,  deficient  in  but  not  free  from 
pigment,  and  relatively  dry  and  bloodless.  Deficient  pigmentation 
may  be  due  to  expectoration  of  inhaled  particles  of  pigment  caught 
in  the  bronchial  excretion  and  its  consequent  failure  to  find  lodgement 
in  the  lung.  Dilatation  of  the  alveoli  and  a  wider  separation  of  those 
particles  deposited  in  the  lungs  may  in  part  account  for  the  appear- 
ance of  deficient  pigmentation. 

In  advanced  cases,  enlarged  vesicles  varying  in  size  from  that  of  a 
pin's  head  to  a  pea  may  be  seen  beneath  the  pleura  or  on  section  within 
the  interior  of  the  lung  in  the  regions  of  most  marked  pulmonary 
involvement.  Coalescence  of  several  cavities  may  lead  to  losses  of 
substance  reaching  the  size  of  a  pigeon's  egg  or  larger.  The  bullae 
are  of  an  irregularly  rounded  or  oval  shape  and  transparent,  and  pro- 
ject (after  the  thorax  is  opened)  above  the  surface  of  the  partially 
retracted  neighboring  tissue.  They  usually  collapse  on  section  and 
present  on  their  inner  surface  the  remnants  of  dilated  and  atrophied 
pulmonary  tissue.  Beneke2  analyzed  the  gas  imprisoned  in  emphy- 
sematous bullae  in  2  cases,  and  found  it  almost  exclusively  nitrogen. 
Alveolar  dilatation  may  be  general  throughout  both  lungs,  but  is 
more  commonly  partial  and  most  marked  at  or  confined  to  the  supra- 
thoracic  or  apical  and  the  sternoparasternal  or  anterior  marginal 
portions.  The  inferior  lateral  parts  are  less  frequently  involved.  The 
central  portions  are  seldom  affected.  Induration  is  absent  unless  the 
condition  is  complicated.  The  weight  of  the  lungs  is  low  compared 
with  their  increased  volume.  The  changes  are  more  obviously  demon- 
strable after  the  lungs  are  distended  and  dried. 

Microscopic  examination  shows  the  alveoli  to  be  enlarged  and  the 
alveolar  walls  atrophied.  In  places,  the  atrophied  septa  about  isolated 
infundibula  have  disappeared,  forming  smaller  vesicles,  while  else- 


1  Beziehung   zwischen   starrer  Thoraxdilatation   und    alveolarem   Lungenemphysem. 
Inaug.  Diss.,  Basel,  1910. 

2  Verhandl.  d.  deut.  Path.  Gesellsch.,  1913,  xvi,  448. 

10 


146  DISEASES  OF   THE  LUNGS 

where  rupture  of  interinfundibular  partitions  has  given  rise  to  larger 
cavities.  The  spaces  thus  formed  may  or  may  not  communicate  with 
normal  or  dilated  bronchi.  The  pulmonary  capillaries  in  the  alveolar 
walls  are  elongated,  straightened,  and  narrowed.  Obliteration  and 
division  of  constricted  vessels  takes  place,  leaving  a  blind  stump  at 
the  point  of  separation.  Consequent  shrinkage  in  the  pulmonary 
circulation  diminishes  the  blood-supply  and  increases  the  work  of  the 
right  ventricle  to  maintain  the  circulation.  Compensatory  dilatation 
of  anastomotic  channels  between  the  pulmonary  arteries  and  the  pul- 
monary and  bronchial  veins  occurs.  Fatty  degeneration  is  observed 
in  the  alveolar  epithelium.  No  essential  changes  have  been  demon- 
strated in  the  elastic  fibers,  which  may,  however,  appear  reduced  in 
size  and  number  owing  to  the  alveolar  dilatation. 

The  bronchi  almost  invariably  show  the  lesions  of  chronic  bronchitis 
with  reddening,  roughening,  and  thickening  of  the  mucous  membrane. 
Atrophy,  dilatation,  and  obliteration  of  the  bronchial  wall  and  peri- 
bronchial induration  may  also  be  found.  Atelectasis,  broncho-,  lobar, 
and  interstitial  pneumonia,  tuberculosis  and  adhesive  pleurisy  may 
be  associated  with  the  emphysema.  Pneumothorax  may  occur  from 
rupture  of  an  emphysematous  bleb. 

As  a  result  of  the  impeded  pulmonary  circulation,  the  pulmonary 
artery  may  become  dilated  and  atheromatous.  At  first  the  right  and 
later  the  left  heart  become  hypertrophied  and  dilated.  Changes  sec- 
ondary to  the  cardiac  failure  take  place  in  other  organs  and  the  patho- 
logic findings  are  those  of  chronic  passive  congestion. 

Symptoms. — The  intensity  of  the  symptoms  depends  on  the  degree 
of  emphysema,  the  condition  of  the  heart,  and  the  severity  of  the 
accompanying  bronchitis.  Dyspnea  and  cough  are  practically  con- 
stant. In  mild  cases,  the  dyspnea  is  present  only  on  exertion.  In 
more  severe  cases,  it  is  persistent  and  aggravated  by  physical  effort, 
intercurrent  attacks  or  exacerbations  of  bronchitis.  In  some  instances 
the  dyspnea  is  of  a  paroxysmal  character  and  may  be  ascribed  to  bron- 
chial or  cardiac  asthma.  Cough  is  due  to  the  accompanying  bronchitis 
and  is  likely  to  be  troublesome,  especially  in  the  early  stages  of  the 
disease.  At  this  period  the  sputum  is  often  scanty,  tough  and  mucoid, 
and  is  raised  with  some  difficulty.  Intervals  of  comparative  freedom 
from  cough  frequently  occur  during  the  summer,  to  be  followed  by 
recurrent  attacks  of  bronchitis  during  the  winter,  and  finally  by  per- 
sistence of  cough  throughout  the  year.  As  the  bronchial  changes 
progress,  the  sputum  becomes  more  abundant  and  less  tenacious,  and 
consists  of  yellowish  purulent  material,  not  infrequently  streaked 
with  blood,  from  the  rupture  of  pulmonary  capillaries  or  passive 
pulmonary  congestion.  Frank  hemorrhages  are  uncommon,  but  may 
occur  from  dilated  bronchial  veins  or  branches  of  the  pulmonary 
arteries.  In  rare  instances  pulmonary  hemorrhages  may  be  fatal. 
With  the  advent  of  cardiac  insufficiency  there  are  such  symptoms 
referable  to  other  systems  as  are  common  in  cardiac  cases. 


DIFFUSE  VESICULAR  EMPHYSEMA  147 

Physical  Signs. — The  findings  on  examination  vary  with  the  degree 
of  emphysema  and  the  condition  of  the  heart.  On  inspection,  cyanosis 
is  seldom  absent,  and  as  in  congenital  cardiac  disease,  may  be  strik- 
ingly out  of  proportion  to  the  accompanying  symptoms.  In  severe 
cases  the  extremities  may  be  cold.  The  expression  is  likely  to  be  anxious 
in  consequence  of  the  dyspnea. 

Respiratory  motion  is  diminished  and  labored  and  the  accessory 
muscles  may  be  brought  into  play.  Inspiration  is  then  accompanied 
by  visible  contraction  of  the  cervical  muscles  and  the  sternocleido- 
mastoids and  the  scaleni  may  be  hypertrophied.  The  arms  and  the 
shoulders  may  be  fixed,  thus  enabling  the  smaller  pectorals  to  take 
part.  Expiration  is  reinforced  by  contraction  of  the  abdominal  muscles 
which  become  tense,  especially  in  the  epigastric  region,  and  form  a 
transverse  furrow  above  the  navel  as  the  patient  expires.  Contraction 
of  the  abdominal  recti  and  the  transversales  narrows  the  lower  thoracic 
aperture  and  displaces  the  abdominal  viscera  and  the  diaphragm 
upward.  The  patient  may  also  resort,  during  expiration,  to  pressure 
of  the  hands  against  the  sides  of  the  chest.  The  thorax  is  enlarged 
in  all  dimensions  as  if  in  a  position  of  permanent  inspiration.  The 
anteroposterior  diameter  is  increased,  giving  the  chest  a  barrel  shape. 
Obliteration  of  the  supraclavicular  fossae  may  occur  from  distention 
of  the  apical  parts  of  the  lungs.  The  neck  looks  short  and  thick,  the 
shoulders  are  high,  the  sternal  fossa  deep,  the  sternum  and  costal 
cartilages  prominent,  the  inferior  intercostal  spaces  widened,  and  the 
lower  thoracic  zone  large.  The  patient  tends  to  bend  forward,  thus 
rounding  the  back. 

The  superficial  veins  may  be  swollen  and  prominent.  The  external 
jugulars,  the  jugular  bulbs,  and  at  times  also  the  upper  thoracic  veins 
may  be  dilated  during  forced  expiration  or  persistently  prominent  and 
further  distended  during  expiration.  In  rare  instances,  a  zone  of  dis- 
tended venules  may  be  seen  on  both  sides  of  the  chest  along  the 
diaphragmatic  attachment. 

In  spite  of  the  increased  respiratory  effort,  thoracic  expansion  is 
less  than  normal.  The  inspiration  is  short  and  quick.  Expiration  is 
long  and  difficult  owing  to  diminished  pulmonary  elasticity.  On 
palpation,  the  tactile  fremitus  is  found  to  be  diminished.  On  percus- 
sion, the  note  is  loud  and  low  pitched,  drum-like  or  hyperresonant. 
The  inferior  limit  of  pulmonary  resonance  may  exceed  by  a  distance 
of  one  to  two  or  more  ribs  the  normal  lower  boundary  of  the  lungs. 
The  amplitude  of  inspiratory  excursion,  determined  by  percussion,  is 
much  diminished  or  absent.  The  distended  lungs  lower  the  upper  limit 
of  hepatic  and  splenic  dulness  and  encroach  upon  the  cardiac  area. 
Traube's  semilunar  space  is  diminished  or  obliterated.  On  ausculta- 
tion, the  breath  sounds  are  feeble  and  often  masked  by  rales  of  the 
sonorous  and  sibilant  variety,  with  which  fine,  medium  or  coarse 
consonating  and  non-consonating  rales  may  also  be  heard.  Prolonga- 
tion of  expiration  is  usually  a  striking  feature. 


148  DISEASES  OF  THE  LUNGS 

Special  Methods  of  Examination. — The  diaphragm  shadow  (Litten's 
phenomenon)  may  be  absent.  When  present,  it  is  of  diminished  ampli- 
tude. Examination  by  means  of  the  .r-rays  show  in  addition  that  the 
diaphragm  is  less  convex  than  normal.  On  inspection  with  the  fluoro- 
scope  the  inspiratory  and  expiratory  changes  in  pulmonary  density 
are  less  marked  than  in  sound  lungs.  Measurement  confirms  the 
increase  in  thoracic  circumference  and  may  show  a  diminution  in  the 
amplitude  of  inspiratory  excursion  after  forced  expiration  from  a  normal 
average  of  about  7  to  4,  2  or  even  1  cm.  Expiratory  pressure  measured 
with  Waldenburg's  pneumotometer1  is  diminished.  The  vital  capacity , 
determined  with  the  spirometer,  may  show  a  reduction  of  from  20  to 
60  per  cent,  below  the  normal.  Riegel's2  pneumographic  tracings  show 
a  diminished  amplitude  for  respiratory  excursion.  The  curves  indicate 
a  rapid  rise  of  inspiration  followed  by  a  rapid  initial  fall  and  a  slow, 
uneven  termination  of  expiration. 

Examination  of  the  Heart. — Pulmonary  distention  makes  the  inves- 
tigation difficult.  The  apex  beat  may  not  be  seen,  but  marked  pul- 
sation may  be  present  in  the  epigastrium  from  depression  of  the  heart 
and  enlargement  of  the  right  ventricle.  The  apex  beat  may  be  palpated 
with  difficulty  or  not  at  all.  On  percussion  the  deep  cardiac  dulness 
may  be  found  increased  laterally  in  consequence  of  hypertrophy  and. 
dilatation,  while  the  upper  limit  may  be  lower  than  normal.  Deter- 
mination of  the  deep  cardiac  dulness  is  often  impossible,  and  the  super- 
ficial dulness  may  be  obliterated.  The  heart  sounds,  although  usually 
of  good  quality,  are  likely  to  be  faint  because  of  the  intervening 
lung.  At  times  a  systolic  blowing  murmur,  due  to  dilatation  of  the 
mitral  ring,  may  be  heard.  The  second  pulmonic  sound  may  be 
accentuated.  An  abnormally  low  position  and  enlargement  of  the 
heart  may  be  confirmed  by  axray  examination.  Cardiac  insufficiency 
is  likely  to  occur  sooner  or  later  in  the  course  of  the  disease  from 
increased  resistance  in  the  pulmonary  circuit.  Diminished  pulmonary 
elasticity  lessens  the  favorable  action  on  the  circulation  of  the  rhythmic 
dilatation  and  retraction  of  the  lung,  and  the  resistance  is  increased 
by  the  heightened  intra-alveolar  pressure  and  atrophy  of  the  capillaries. 
Compensation  is  at  first  affected  by  hypertrophy  of  the  right  side, 
which  later  becomes  dilated  and  insufficient.  As  the  cardiac  nutrition 
suffers,  the  left  side  becomes  involved,  and  the  clinical  aspect  is  then 
that  of  broken  cardiac  compensation,  with  weak  and  irregular  heart 
sounds,  pulmonary  edema,  hydrothorax,  enlargement  of  the  liver, 
ascites,  edema  of  the  feet,  and  passive  congestion  of  the  kidney. 

The  blood  shows  no  distinctive  features  in  emphysema.  Such 
variations  from  the  normal  as  occur  may  be  ascribed  to  cardiac  decom- 
pensation, in  the  first  stages  of  which,  as  noted  by  Grawitz3  the  number 

1  Die  pneumatische  Behandlung  der  Respirations-  und  Zirkulations-krankheiten, 
Berlin,  1875. 

2  Deut.  Arch.  f.  klin.  Med.,  Bd.  x,  p.  124. 

3  Klin.  Path,  des  Blutes,  Leipzig,  1906. 


DIFFUSE  VESICULAR  EMPHYSEMA  149. 

of  red-blood  corpuscles  and  the  amount  of  hemoglobin  are  diminished. 
As  the  cardiac  failure  becomes  more  chronic  with  dyspnea,  cyanosis 
and  edema,  the  blood  becomes  more  concentrated  with  increase  in 
the  number  of  red-blood  corpuscles. 

Diagnosis. — When  of  slight  degree,  emphysema  is  likely  to  escape 
detection.  Outspoken  cases  are  easily  recognized  from  the  dyspnea 
and  cyanosis,  bronchial  catarrh,  enlargement  and  shape  of  the  thorax, 
diminished  and  labored  respiratory  motion,  hyperresonance,  depres- 
sion of  the  inferior  pulmonary  margins,  diminished  area  of  cardiac 
dulness,  feeble  breath  sounds,  prolonged  expiration  and  diminished 
but  not  absent  tactile  fremitus.  Acute  pulmonary  distention  is  to  be 
distinguished  from  the  chronic  form  by  a  history  of  recent  onset, 
only  moderate  inflation  seldom  exceeding  the  limits  of  full  inspiration 
and  a  tendency  to  subside  within  a  limited  period  of  a  few  hours  or 
days.  With  pneumothorax  there  is  hyperresonance,  feeble  breath 
sounds,  and  diminished  or  absent  tactile  fremitus,  but  the  limitation 
of  these  signs  to  a  circumscribed  area,  the  presence  of  metallic  tinkle, 
coin  sound,  succussion  and  dislocation  of  the  heart  will  serve  to  dis- 
tinguish it.  If  the  patient  is  first  seen  in  the  later  stages  when  the  heart 
has  failed,  the  cardiac  features  may  dominate  the  clinical  picture. 
In  extreme  cases,  passive  congestion  of  the  lung,  hydrothorax  and 
hydropericardium  may  then  mask  the  signs  of  emphysema.  Unless 
a  history  of  emphysema  can  be  obtained  and  other  cardiac  or  extra- 
cardiac  causes  of  cardiac  insufficiency  be  excluded,  the  diagnosis  may 
be  impossible. 

Emphysema  may  in  turn  make  the  detection  of  an  underlying 
pulmonary  tuberculosis  difficult  or  impossible,  but  the  history  may 
suggest  tuberculosis  and  evidence  of  apical  disease  may  still  be  de- 
monstrable. Apical  retraction  may  depress  one  or  the  other  supra- 
clavicular fossse  or  restrict  the  degree  to  which  this  region  is  inflated 
when  the  patient  coughs.  Physical  signs  of  apical  disease  may  be 
accentuated  by  examination  while  the  breath  is  held  in  full  inspiration. 

Prognosis. — Owing  to  the  anatomic  changes  in  chronic  diffuse 
emphysema,  return  of  the  lung  to  normal  cannot  be  expected.  In 
rare  instances  the  disease  may  become  stationary.  More  commonly, 
however,  it  slowly  and  steadily  progresses  and  lasts  a  long  time,  but 
shortens  life  by  many  years.  In  a  majority  of  cases,  the  capacity 
for  physical  work  is  considerably  diminished. 

Owing  to  the  usual  presence  of  a  chronic  bronchial  and  broncho- 
pulmonary infection,  patients  with  the  disease  are  in  danger  of  acute 
exacerbations  with  extension  of  inflammation  to  previously  uninvolved 
regions.  An  acute  bronchopneumonia,  pulmonary  abscess  or  gangrene 
may  thus  arise.  Invasion  of  the  pleura  may  cause  an  acute  or  chronic 
pleurisy  with  or  without  exudation.  In  rare  instances,  rupture  of  an 
emphysematous  bleb  may  cause  pneumothorax.  It  is  doubtful  if 
emphysema  exerts  a  restraining  influence  on  pulmonary  tuberculosis. 
It  seems  probable  that  the  emphysema  associated  with  long-standing 


150  DISEASES  OF  THE  LUNGS 

phthisis  is  rather  the  result  of  the  accompanying  nutritive  and  mechan- 
ical disturbance  than  a  cause  of  the  chronicity  of  the  tuberculous 

process.  The  infrequency  with  which  the  two  are  associated  may  be 
due  to  the  more  frequent  occurrence  of  tuberculosis  in  early  and  of 
emphysema   in.  later  life. 

Aside  from  complications  which  may  more  or  less  suddenly  terminate 
the  slow  progress  of  the  disease,  the  outlook  depends  for  the  most  part 
on  the  degree  to  which  the  circulatory  system  has  suffered  from  the 
pulmonary  disturbance.  In  estimating  the  probable  expectation  of  life 
in  any  individual  case,  the  duration  of  the  disease,  the  degree  of  dysp- 
nea and  cyanosis,  the  amount  of  bronchitis,  extent  of  the  cardiac 
embarrassment,  the  age,  strength,  general  nutrition  and  opportunity 
for  limiting  physical  exertion  must  be  taken  into  consideration.  The 
condition  is  more  likely  to  progress  only  slowly  when  the  pulmonary 
features  are  mild,  the  bronchial  catarrh  stationary  and  uninterrupted 
by  exacerbations,  without  cardiac  weakness,  with  a  strong  constitution 
and  under  circumstances  which  admit  of  proper  regulation  of  the 
daily  life. 

Functional  tests  of  the  pulmonary  capacity  may  be  of  assistance 
in  estimating  the  prognosis.  The  vital  respiratory  capacity  for  a  man 
of  average  height  may  be  estimated  at  somewhat  more  than  3000  c.c. 
Waldenburg  regards  a  capacity  under  two  liters  as  indicating  a  severe 
case.  Considerable  diminution  of  the  average  normal  difference  of  7 
cm.  between  the  thoracic  circumference  at  the  end  of  forced  inspiration 
and  at  the  end  of  forced  expiration,  the  measurement  being  taken  at 
the  level  of  the  nipple,  may  have  a  similar  import. 

Treatment. — This  should  be  directed  against  the  bronchitis,  the 
cardiac  weakness,  when  this  is  present,  and  the  emphysema  itself. 

The  treatment  of  the  bronchitis  need  not  be  fully  considered  here. 
The  patient  may  well  be  cautioned  against  exposure  to  cold  or  draught 
when  overheated  or  insufficiently  clad.  Expectorants  are  at  times  of 
value,  and  sedatives  may  be  used  when  sleep  is  disturbed  by  harassing 
and  ineffectual  cough.  Partial  inversion,  as  in  the  treatment  of  bron- 
chiectasis, may  be  of  service  in  clearing  the  bronchi  of  stagnating  secre- 
tion. Measures  which  improve  the  general  health  are  of  importance. 
Cool  morning  baths  followed  by  a  rub  with  a  harsh  towel,  an  abundance 
of  nourishing  food  and  fresh  air  by  night  as  well  as  by  day  may  be 
recommended.  An  accompanying  asthma  should  be  appropriately 
treated  and  the  nose  examined  for  sources  of  reflex  irritation.  Gastro- 
intestinal disturbances  should  be  corrected.  Flatus  is  to  be  avoided. 
A  light  evening  meal  may  render  the  nights  more  comfortable.  The 
bowels  should  be  kept  regular.  When  necessary,  a  change  to  an  equable 
climate  and  an  atmosphere  free  from  dust  are  to  be  considered. 
Country  is  better  than  city  life. 

Cardiac  weakness  is  to  be  combated  by  rest,  limitation  of  food, 
liquids,  and  salt,  the  use  of  digitalis  and  other  appropriate  means. 
Venesection  is  justifiable  when  there  is  urgent  dyspnea,  intense  cya- 


DIFFUSE   VESICULAR  EMPHYSEMA  151 

nosis,  venous  engorgement,  and  overfilling  of  the  right  heart.  It  may 
then  prove  a  life-saving  measure.  Inhalations  of  oxygen  may  be  help- 
ful.   Camphor  and  caffein  may  also  be  used. 

The  treatment  of  the  emphysema  is  unsatisfactory.  The  inelastic 
and  atrophied  pulmonary  tissue  cannot  be  returned  to  its  normal 
condition.  Such  simple  measures  as  rhythmic  compression  of  the  two 
sides  of  the  thorax  with  the  hands  during  expiration  may  be  of  service. 
Rossbach1  recommended  mechanical  in  place  of  manual  compression. 
Hoffmann2  recommends  respiratory  exercises.  All  tight  clothing 
should  be  removed.  The  patient  holds  in  each  hand  a  light  dumbbell 
(one  pound)  and  raises  the  arms  from  the  sides  to  a  horizontal  position. 
The  hands  are  then  brought  into  supination,  with  the  palm  upward, 
and  at  the  same  time  an  inspiration  is  taken.  The  movements  are 
then  reversed,  the  hands  returned  to  the  side  of  the  body,  and  the 
knees  bent  until  the  dumbbells  touch  the  floor.  During  this  move- 
ment the  patient  expires.  He  regards  six  inspiratory  movements  of 
this  sort  as  sufficient  for  most  emphysematous  patients.  Treatment 
by  means  of  the  pneumatic  cabinet  is  sometimes  used.  With  the  patient 
in  the  cabinet  the  air  pressure  is  gradually  raised,  during  a  period  of 
about  a  half-hour,  to  one  and  one-half  to  two  atmospheres.  The 
compressed  air  is  breathed  for  one-half  to  one  hour  and  the  pressure 
then  gradually  lowered  to  normal,  another  half-hour  being  consumed 
in  the  process  of  reduction.  Active  pneumatic  treatment  can  be  carried 
out  by  means  of  portable  apparatus,  such  as  Waldenburg's  or  its 
modifications.  The  patient  may  inspire  air  under  a  positive  pressure 
of  one-sixtieth  to  one-fiftieth  of  an  atmosphere  or  expire  into  air 
rarefied  to  a  negative  pressure  of  from  one-sixtieth  to  one  twenty- 
fifth  of  an  atmosphere.  Treatment  by  means  of  Zander  apparatus, 
by  simple  or  concussion  massage,  and  by  hydrotherapy  has  also  been 
used.  A  cure  cannot  be  expected,  but  some  at  least  temporary  allevia- 
tion of  symptoms  may  be  accomplished  by  these  various  means. 

Hofbauer3  instructs  his  patients  to  avoid  any  increase  of  inspiration 
and  to  prolong  expiration,  during  which  the  accessory  expiratory 
muscles  of  the  abdomen  are  brought  into  play.  During  the  first  part 
of  the  treatment  an  apparatus  is  used  which  exerts  automatic,  rhythmic 
pressure  on  the  abdomen  during  expiration.  After  some  practice 
with  the  apparatus,  the  patient  learns  to  use  his  abdominal  muscles 
without  such  assistance  during  expiration. 

Freund's  theory  of  the  origin  of  emphysema  in  degenerative  changes, 
calcification  and  loss  of  elasticity  in  the  costal  cartilages  has  led  to 
his  recommendation  of  surgical  measures  for  its  relief.  Unilateral 
or  bilateral  incision,  combined  usually  with  partial  excision  of  the  calci- 

1  Ueber  einen  Atmungsstuhl  fur  Emphysematiker,  Verhandl.  d.  VI  Kongress.  f. 
inn.  Med.,  Wiesbaden,  1887,  p.  217. 

2  Nothnagel's  Encyclopedia  of  Practical  Medic.  Diseases  of  the  Bronchi,  Pleura,  and 
Lungs,  p.  353. 

3  Wiener  med.  Woch.,  1908,  No.  6,  p.  289. 


152  DISEASES  OF  THE  LUNGS 

tied  costal  cartilages,  has  been  performed  in  a  considerable  number 
of  cases,  and  almost  constantly  with  relief  of  the  dyspnea  and  an 
increased  capacity  for  physical  exertion.  The  future  of  this  procedure 
cannot  yet  be  judged. 

2.  ACUTE    VESICULAR   EMPHYSEMA. 

This  is  also  known  as  acute  pulmonary  inflation.  It  is  the  volumen 
pulmonis  auctum  of  Traube,  and  is  most  frequent  in  connection  with 
asthmatic  attacks,  but  may  occur  also  in  consequence  of  whooping 
cough,  croup,  capillary  bronchitis,  laryngeal  diphtheria,  the  inhalation 
of  irritating  gases,  suffocation  by  strangulation,  pulmonary  edema 
or  foreign  bodies  in  the  air  passages.  In  these  conditions,  strong 
inspiratory  efforts  are  followed  by  forced  expiration  against  the  closed 
glottis  when  the  patient  coughs.  The  lungs  are  thus  increased  in  size 
and  the  air  vesicles  become  much  distended.  Acute  pulmonary  dis- 
tention occurring  in  normal  individuals  after  deep  breathing  or  physical 
exertion,  or  in  dyspnea,  air-hunger,  and  cardiac  insufficiency  may  be 
mentioned  in  this  connection,  and  is  probably  due  to  inspiratory  over- 
distension with  persistence  in  the  lungs  of  an  abnormal  amount  of 
residual  air.  These  forms  of  acute  pulmonary  distention,  as  well  as 
those  produced  experimentally  in  animals,  have  already  been  discussed 
under  Pathogenesis  in  the  preceding  section.  In  many  instances, 
the  condition  is  transient  and  subsides  with  the  removal  of  the  cause. 
Repeated  or  persistent  overdistention,  however,  in  association  with 
impairment  of  pulmonary  nutrition,  may  lead  to  chronic  emphysema. 

3.  COMPENSATORY  EMPHYSEMA. 

This  is  also  termed  vicarious,  collateral,  complementary  or  partial 
emphysema.  The  condition  is  of  pathologic  rather  than  of  clinical 
interest,  as  it  is  usually  limited  to  the  neighborhood  of  processes  which 
occupy  the  foreground  in  the  clinical  picture,  and  so  mask  the  situation 
as  to  make  its  detection  during  life  difficult  or  impossible.  It  occurs 
in  the  neighborhood  of  atelectatic,  inflamed  or  contracted  parts  of  the 
lung,  and  may  thus  be  associated  with  pleurisy  with  effusion  or  pneu- 
mothorax, simple  or  tuberculous  bronchopneumonia,  extensive  pleural 
adhesions,  pulmonary  cicatrices  or  areas  of  interstitial  pneumonia. 
Imperfect  expansion  of  the  airless,  inflamed  or  contracted  pulmonary 
tissue  may  be  compensated  either  by  depression  of  the  chest  wall  or 
overinflation  of  the  adjacent  pulmonary  tissue.  If  the  area  of  diseased 
lung  tissue  excluded  from  participation  in  respiratory  motion  is  of  large 
extent,  thoracic  retraction  and  compensatory  emphysema  may  both 
result.  The  larger  the  area  of  diseased  lung,  the  greater  the  extent  of 
the  emphysema.  Thus  extensive  contraction  of  one  may  cause  emphy- 
sema of  the  other  lung.  The  persistence  of  the  process  depends  on  the 
duration  of  the  cause.    If  this  is  of  short  duration,  an  acute  pulmonary 


INTERSTITIAL  EMPHYSEMA  153 

inflation  only  may  result,  and  this  may  subside  with  the  subsidence 
of  the  cause.  In  chronic  cases,  however,  persistent  overdistentioD 
is  followed  not  only  by  enlargement  and  rarefaction  of  the  air  vesicles, 
but  also  by  atrophy  of  the  tissue.  Aside  from  the  limited  extent  of 
the  process,  the  pathologic  picture  does  not  differ  from  that  in  the 
diffuse  form  of  the  disease.  The  dilatation  and  atrophy  of  the  affected 
region  impair  its  respiratory  capacity  and  may  thus  aggravate  symp- 
toms due  to  the  underlying  cause.  In  cases  in  which  the  emphysema 
is  demonstrable,  the  physical  signs  are  those  already  described  for  the 
diffuse  form. 

4.  SENILE   EMPHYSEMA. 

This  form,  also  termed  atrophic  emphysema,  is  an  involution  process 
of  advancing  age  in  which  the  lung  shares  the  wasting  taking  place 
in  other  parts  of  the  body.  Pulmonary  elasticity  is  diminished  and  the 
lung  in  consequence  more  nearly  assumes  a  permanent  inspiratory 
position.  The  condition  differs  from  the  preceding  forms  in  that  the 
thorax  and  the  lung  are  diminished  rather  than  increased  in  size. 
There  is  likely  to  be  kyphosis  of  the  dorsal  region  of  the  spine,  lateral 
narrowing  of  the  thorax  and  a  diminished  width  of  the  intercostal 
spaces.  Respiratory  motion  is  diminished,  the  inferior  pulmonary 
margins  are  high  rather  than  low,  and  the  area  of  cardiac  dulness  is 
not  decreased.  According  to  Tendeloo  the  emphysema  first  makes 
its  appearance  and  is  most  pronounced  in  the  sternoparasternal  and 
lateral  caudal  parts  of  the  lungs,  while  the  suprathoracic  portions  are 
more  or  less  involved  in  consequence  of  chronic  bronchitis  so  frequently 
present  in  the  aged. 

5.  INTERSTITIAL  EMPHYSEMA. 

This  is  also  known  as  interlobular  emphysema  and  occurs  when  air 
enters  the  interstitial  tissue  of  the  lung  following  rupture  of  the  bron- 
chial mucous  membrane  or  the  alveolar  septa.  The  condition  was 
described  by  Laennec,1  and  has  been  studied,  principally  in  connection 
with  mediastinal  emphysema,  among  others  by  Roger,2  Bartels,3 
Cruveilhier,4  Fr.  Muller,5  and  Frankel.6 

Interstitial  emphysema  is  most  common  in  children  and  youthful 
adults.  It  is  usually  due  to  greatly  increased  expiratory  pressure 
during  a  severe  paroxysm  of  cough,  and  may  thus  occur  in  whooping 
cough,  laryngeal  stenosis  from  diphtheria,  in  broncho-  or  lobar  pneu- 
monia, pulmonary  abscess,  gangrene  or  tuberculosis.  Fraentzel7 
described  2  cases  (one  with  autopsy)  in  which  it  occurred  in  the  stage 

1  Traite  de  l'auscultation  mediate,  1831,  T.  i,  Troisieme  edition,  p.  324. 

2  Arch.  gen.  de  med.,  1862,  T.  ii,  p.  129. 

3  Deut.  Arch.  f.  klin.  Med.,  vol.  ii,  p.  392. 

4  Gaz.  hebd.  de  med.  et  de  chir.,  1856,  p.  179. 

»  Berl.  klin.  Woch.,  12  Marz,  1888.  6  Ibid.>  24  Okt.,  1910. 

7  Dent.  med.  Woch.,  12  Marz,  1885,  No.  11,  p.  162. 


154  DISEASES  OF  THE  LUNGS 

of  asphyxia  in  cholera,  as  he  believed  in  consequence  of  the  severe 
grade  of  dyspnea.  It  may  also  occur  during  parturition,  from  strangu- 
lation or  result  from  too  forcible  insufflation  or  undue  force  in  perform- 
ing artificial  respiration  for  the  resuscitation  of  patients  in  a  condition 
of  asphyxia.  A  stab  or  bullet  wound,  a  contusion  or  blow  may  be  the 
cause.  Laceration  of  the  lung  may  take  place  without  external  evi- 
dence of  the  injury.  It  may  follow  severe  or  mild  exertion,  and  in 
rare  instances  is  apparently  of  spontaneous  origin.  In  such  cases, 
however,  some  pathologic  condition  may  fairly  be  assumed.  Latent 
pulmonary  tuberculosis,  the  rupture  of  an  emphysematous  bleb  or 
pleural  adhesion  are  then  possible  causes. 

On  examination  of  a  lung  infiltrated  with  air,  transparent,  sharply 
circumscribed,  parallel  or  intersecting  lines  or  bands  may  be  seen 
through  the  pleura  in  the  interlobular  tissue.  They  are  likely  to  be 
most  numerous  toward  the  margins  of  the  lung,  and  may  coalesce  to 
form  bubbles  of  considerable  size.  The  appearance  may  be  not  unlike 
that  of  a  string  of  beads.  The  air  spaces  diminish  in  size  toward 
the  centre  of  the  lung,  and  according  to  Laennec,  are  wedge-shaped 
like  the  segments  of  an  orange  with  the  base  of  the  wedge  toward  the 
pleura.  The  air  may  pass  by  way  of  the  interlobular  connective  tissue 
along  the  bronchi,  or  bloodvessels,  or  by  way  of  the  subpleural  con- 
nective tissue  to  the  hilus  of  the  lung ,  thence  to  the  anterior  or  posterior 
mediastinum  and  the  subcutaneous  tissue  of  the  neck.  If  an  unadherent 
pleura  is  ruptured,  a  pneumothorax  results.  If  adherent  pleural 
layers  are  ruptured,  the  air  may  pass  directly  to  the  thoracic  subcu- 
taneous tissue.  Mediastinal  or  subcutaneous  emphysema  of  pulmonary 
origin  is  not  necessarily  associated  with  interstitial  emphysema,  since 
it  may  arise  from  laceration  at  the  root  or  periphery  of  the  lung 
directly  into  the  mediastinal  or  subcutaneous  tissue  through  an 
adherent  pleura. 

Distinctive  clinical  features  are  lacking  with  interstitial  and  sub- 
pleural emphysema.  Dyspnea  and  cyanosis  may  result  from  the  limi- 
tation of  respiratory  surface.  Laennec  regarded  a  coarse,  dry,  crepi- 
tant rale  (rale  crepitant  sec  a  grosses  bulles)  as  pathognomonic  of  inter- 
lobular emphysema.  He  stated  that  an  inspiratory  and  expiratory 
friction  rub  (frottement  ascendant  et  descendant)  was  also  usually 
present.  His  observations  have  not  since  been  confirmed.  Cruveil- 
hier  and  Miiller  have  noted  the  masking  or  modification  by  sub- 
pleural emphysema  of  auscultatory  signs  previously  present.  The 
diagnosis  of  interstitial  or  subpleural  emphysema  can  usually  be  made, 
however,  only  by  inference  and  the  presence  of  a  complicating  medias- 
tinal or  subcutaneous  emphysema  or  a  pneumothorax.  Because  of 
its  importance  in  this  connection,  mediastinal  emphysema  will  be 
further  considered. 

Mediastinal  Emphysema. — As  already  stated,  this  may  be  due  to 
the  passage  of  air  from  the  interstitial  or  subpleural  tissue  to  the 
root  of   the  lung  and  thence  to  the  mediastinum.      It  may   also 


INTERSTITIAL  EMPHYSEMA  155 

arise  from  perforation  of  the  root  or  peripheral  parts  of  the  lung 
adjacent  to  the  mediastinum.  Laceration  of  the  trachea  or  the 
esophagus  or  extension  downward  of  subcutaneous  emphysema  in  the 
cervical  regions  are  also  causes.  An  origin  from  the  lung  is  most  com- 
mon. The  air  infiltrates  the  loose  mediastinal  tissue.  It  may  surround 
the  pericardium  and  great  vessels,  the  trachea  and  esophagus,  separate 
the  costal  pleura  from  the  ribs  for  a  short  distance  laterally,  extend 
downward  as  far  as  the  insertion  of  the  diaphragm,  and  upward  along 
the  trachea  or  the  great  vessels  to  the  subcutaneous  tissue  of  the  neck. 
Here  it  may  appear  as  a  crepitating  tumor  in  the  supraclavicular 
region  and  more  commonly  on  the  left  than  on  the  right  side.  From 
this  region  it  may  spread  to  other  parts  of  the  body. 

There  may  be  pain  or  a  sense  of  oppression  referred  to  the  precordial 
region,  and  increased  by  deep  inspiration.  Existing  dyspnea  may  be 
aggravated.  Dysphagia  and  changes  in  the  voice  have  been  described. 
On  examination,  the  deep  cardiac  dulness  may  be  absent,  the  super- 
ficial cardiac  dulness  very  much  reduced  or  entirely  replaced  by  a 
resonant  note  with  or  without  a  tympanitic  quality.  Mediastinal 
resonance  may  extend  to  the  right  as  far  as  the  parasternal  line,  to  the 
left  to  or  beyond  the  nipple  line,  and  downward  to  or  beyond  the  costal 
margin  in  the  sternal  region,  meeting  here  the  liver  dulness.  The 
precordial  resonance  does  not  change  on  changing  the  position  of  the 
patient.  The  cardiac  impulse  is  usually  almost  or  quite  invisible 
and  impalpable.  The  most  important  sign  is  the  presence  of  a  fine 
crepitation  over  the  cardiac  region,  heard  during  both  systole  and 
diastole,  usually  of  maximum  intensity  during  the  former,  at  times 
increased  during  inspiration  and  present  when  the  breath  is  held. 
The  cardiac  sounds  may  be  normal,  faint,  masked  by  the  crepitation 
or  inaudible.  Peterson1  and  Schotten2  have  each  described  as  extra- 
pericardial  emphysema  a  case  in  which  a  splashing  or  whirring  sound 
could  be  heard  at  a  distance  from  the  patient,  but  in  these  cases 
pneumopericardium  could  hardly  be  excluded.  Mediastinal  emphy- 
sema shares  in  common  with  pneumopericardium  a  resonant  or  tym- 
panitic precordial  percussion  note,  but  with  the  latter  precordial 
dulness  may  be  elicited  when  the  patient  is  bent  forward  so  as  to 
bring  the  heart  against  the  chest  wall,  and  owing  to  the  usual  presence 
of  both  fluid  and  air  in  the  pericardial  sac,  there  are  likely  to  be  loud, 
splashing,  gurgling  or  churning  sounds  (bruit  de  moulin,  or  better, 
bruit  de  roue  hydraulique,  as  suggested  by  Morel-Lavallee3)  rather 
than  a  fine  crepitation.  Pneumothorax  must  be  excluded.  When 
pneumothorax  is  present,  the  precordia  may  be  resonant  or  tym- 
panitic, but  physical  examination  assisted,  if  necessary,  by  the  re-rays, 
will  usually  show  the  heart  displaced  toward  the  unaffected  side,  the 
absence  of  precordial  crepitation  in  uncomplicated  cases,  and,  in 
addition,  unilateral  limitation  of  respiratory  motion,  enlargement  of 

1  Berl.  klin.  Woch.,  1884,  p.  699.  -  Ibid.,  1886,  p.  882. 

3  Gaz.  med.  de  Paris,  12  Nov.,  1864,  No.  46. 


15G  DISEASES  OF  THE  LUNGS 

the  side,  hyperresonance,  diminished  or  absent  fremitus  and  breath- 
ing, metallic  phenomena,  and  succussion  over  the  anterolateral  or 
posterior  parts  of  the  chest. 

The  prognosis  is  in  general  that  of  the  underlying  disease,  since 
interstitial,  with  or  without  mediastinal  and  subcutaneous  emphysema, 
adds  only  little  to  the  gravity  of  the  situation,  although  this  may  be 
enough  in  already  desperate  cases  to  hasten  a  fatal  termination  from 
the  added  burden  to  the  heart  and  the  lung.  In  favorable  cases,  the 
air  is  usually  absorbed  in  from  one  to  three  weeks.  Treatment  should 
be  directed  toward  preventing  an  aggravation  of  the  condition  by  an 
elevation  of  intrapulmonary  tension.  Rest  in  bed  and  suppression  of 
cough,  if  necessary,  by  sedatives  usually  suffice. 


CHAPTER  X. 
LOBAR  PNEUMONIA. 

Occurrence. — The  frequency  of  pneumonia  in  comparison  with  all 
internal  diseases  is  usually  estimated  at  from  about  3  to  6  per  cent. 
Among  32,616  medical  admissions  at  the  Massachusetts  General 
Hospital,  from  1897  to  1913,  were  2025  cases  (6.2  per  cent.)  of  lobar 
pneumonia. 

In  the  United  States,  for  the  census  year  1890,  over  9  per  cent,  of 
all  deaths  were  due  to  pneumonia,  in  1900  over  10  per  cent,  and  in  1909 
9.5  per  cent.  The  annual  average  death  rate  from  lobar  pneumonia 
per  100,000  population  from  1900  to  1909  in  the  registration  area  was 
117.6,  but  there  has  been  a  fairly  steady  decline  from  158.6  in  1900 
to  96.3  in  1909.  In  the  registration  cities,  the  annual  average  was 
131.4,  with  a  decline  from  177.9  in  1900  to  107.7  in  1909.  The  death 
rate  is  lower  in  the  rural  districts  of  the  registration  area,  amounting 
to  an  annual  average  of  90.4,  with  a  similar  diminution  in  the  mortality 
from  113.9  in  1900  to  80.4  in  1909. 

Predisposing  Influences. — These  may  be  divided  into  general  and 
individual  factors. 

General  Factors. — (a)  Geographic. — Pneumonia  occurs  in  all  parts 
of  the  world,  but  appears  to  be  more  frequent  in  temperate  regions. 
Altitude  does  not  seem  to  be  a  factor  of  importance. 

(b)  Racial. — Pneumonia  has  not  infrequently  been  noted  to  be 
more  prevalent  and  more  severe  among  negroes  than  among  whites. 
Gorgas1  states  that  in  1906,  in  an  average  force  of  21,000  negroes 
employed  in  the  construction  of  the  Panama  Canal,  there  were  396 
deaths  from  pneumonia,  giving  a  death  rate  of  18.74  per  thousand. 
In  1907,  in  an  average  force  of  28,600  negroes,  there  were  304  deaths 
from  pneumonia,  a  death  rate  of  10.65.  A  high  rate  of  mortality  from 
pneumonia  has  similarly  been  observed  among  the  negroes  employed 
in  the  mines  of  the  Rand.  For  the  year  1912  among  21,000  tropical 
natives  the  death  rate  from  pneumonia  was  26.30,  while  among  199,000 
non-tropicals  the  death  rate  was  only  8.  Both  in  Panama  and  in  the 
Rand  it  has  been  noted  that  the  highest  mortality  occurs  among  the 
recent  arrivals  and  that  the  mortality  rapidly  diminishes  after  a  short 
residence  in  the  community.  Thus  it  was  found  at  Panama  that 
pneumonia  was  four  and  one-half  times  as  frequent  among  the  men 
who  had  been  on  the  Isthmus  less  than  three  months,  as  it  was  among 

1  Jour.  Amer.  Med.  Assoc,  1914,  lxii,  p.  1855. 


158  DISEASES  OF  THE  LUNGS 

those  in  residence  more  than  three  months.  A  striking  diminution  in 
the  mortality  from  pneumonia  has  been  observed  among  the  negroes 
employed  on  the  Isthmian  ("anal  in  the  years  succeeding  1907,  the 
death  rate  not  exceeding  2.60  for  any  year  up  to  and  including  1912. 
The  importance  of  race  is  difficult  to  estimate  and  it  seems  probable 
that  apparent  racial  susceptibility  is  largely  due  to  lack  of  acquired 
immunity.  An  initial  susceptibility  may  be  due  to  lack  of  exposure 
to  virulent  strains  of  the  pneumococcus  and  the  protective  influence 
of  minor  pneumococcus  infections  of  the  upper  parts  of  the  respiratory 
tract. 

(c)  Meteorological. — Marked  variation  in  temperature,  small  amount 
of  rainfall,  and  high  winds  have  been  thought  to  increase  the  incidence 
of  pneumonia,  but  no  constant  relation  with  these  influences  has  been 
shown.  A  seasonal  influence  is  the  only  factor  which  can  be  affirmed 
in  this  group.  In  practically  all  large  series  of  cases  it  has  been  shown 
that  the  majority  of  cases  occur  in  the  months  between  November 
and  June,  but  with  some  difference  in  the  predominance  of  cases  in 
different  countries  during  the  winter  or  spring  months.  An  estimate 
of  the  importance  of  wind,  weather  and  seasonal  conditions  is  ren- 
dered difficult  by  the  entrance  into  the  problem  of  such  other  factors 
as  the  tendency  of  the  people  to  live  under  less  satisfactory  hygienic 
conditions,  in  crowded  and  poorly  ventilated  rooms,  during  inclement 
weather. 

(d)  Increased  Virulence  of  the  Organisms. — Variation  in  virulence  of 
the  pneumococcus  obtained  from  different  sources  can  readily  be  estab- 
lished by  animal  experimentation  in  the  laboratory.  The  virulence 
of  an  organism  can  be  raised  and  maintained  only  by  frequent  trans- 
plantation on  suitable  media  and  the  passage  at  proper  intervals 
through  susceptible  animals.  An  increase  in  virulence  probably 
occurs  by  passage  through  man  as  well  as  through  animals,  and  the 
chances  for  infection  of  those  exposed  are  greatly  increased  by  the 
presence  of  a  highly  virulent  strain.  A  relatively  insusceptible  person 
may  act  as  a  carrier  without  himself  becoming  infected. 

(e)  Epidemics. — Pneumonia  is  to  be  regarded  rather  as  an  endemic 
than  as  an  epidemic  disease,  but  numerous  instances  can  be  cited  of 
more  or  less  severe  local  outbreaks.  Wells1  presents  a  chronological 
table  of  epidemics  from  1440  to  1888.  They  have  occurred  in  all  parts 
of  the  world,  and  most  often  during  the  winter  and  spring  months. 
Certain  outbreaks  have  presented  special  peculiarities.  That  at  Ober 
Sichte  in  1880  was  confined  to  children  under  five,  of  whom  15  out  of 
50  were  attacked.  The  epidemic  in  Alaska  in  1881  affected  the  native 
population  almost  exclusively  and  was  very  fatal.  In  Rietnordhausen, 
in  1881,  of  700  inhabitants,  42  were  attacked  with  only  two  deaths, 
a  strikingly  low  mortality.  Numerous  epidemics  on  board  ships  have 
been  recorded.   In  1863,  the  disease  broke  out  on  H.  M.  Ships  St.  Jean 

1  Jour.  Amcr.  Med.  Assoc,  February  26,  1889. 


LOBAR  PNEUMONIA  159 

d'Acre  and  Cressy,  attacking  410  of  815  persons  on  the  former  and  298 
of  720  on  the  latter.  Of  epidemics  in  jails,  that  at  Moringen1  in  1878 
is  most  often  noted.  Of  between  700  and  900  inmates,  58  were  affected. 
Kerschensteiner2  reported  that  of  1150  prisoners  at  Amberg,  101  had 
pneumonia,  and  40  died  during  the  first  five  months  of  the  year  1880. 
Epidemics  in  barracks  have  been  frequently  reported.  Of  hospital 
outbreaks,  that  recorded  by  Edsall  and  Ghriskey3  is  most  instructive. 
Within  eleven  days  following  the  death  of  a  patient  in  a  certain  bed 
in  the  Episcopal  Hospital  at  Philadelphia,  two  patients  temporarily 
placed  in  the  same  bed,  developed  pneumonia,  and  on  the  twelfth 
day  pneumococci  were  found  in  the  blood  of  a  patient  in  a  neighboring 
bed,  but  evidence  of  pneumonia  failed  to  develop. 

A  succession  of  cases  in  the  same  house  has  occasionally  been  noted, 
and  Jiirgensen4  offers,  in  support  of  his  opinion  that  pneumonia  is  a 
house  disease,  the  experience  at  Lustgau  where  in  223  dwellings, 
during  an  interval  of  eight  years,  the  disease  occurred  once  in  40, 
several  times  in  44,  and  not  at  all  in  139.  One  of  the  most  striking 
instances  of  house  infection  is  reported  by  Schroeder,5  who  found  that 
34  cases  had  come  to  the  local  clinic  at  Kiel  from  one  house  during  an 
interval  of  fourteen  years.  Kuhn6  gives  a  striking  example  of  apparent 
contagion  from  person  to  person.  A  man  of  seventy-six  was  attacked 
by  pneumonia.  On  the  third  day  of  his  illness  his  wife,  who  slept 
in  the  same  bed,  was  taken  with  the  disease  and  died  on  the  second 
day,  her  husband  dying  a  day  later,  i.  e.,  the  sixth  day  of  his  illness. 
A  daughter  forty  years  of  age,  who  lived  at  the  other  end  of  the  village 
and  came  as  often  as  possible  to  visit  her  parents  and  watch  over 
them  at  night,  was  taken  ill  with  pneumonia  on  the  same  day  as  her 
mother.  She  also  died.  On  the  day  his  parents  were  buried  a  son, 
aged  thirty-two  years,  who  lived  with  them,  had  a  chill  and  elevation 
of  temperature  which  subsided  the  next  day  without  pulmonary 
manifestations.  At  almost  the  same  time  his  half-year-old  child  had 
an  eclamptic  attack,  with  high  fever,  and  developed  a  catarrhal 
pneumonia  which  ran  a  favorable  course. 

An  increase  in  the  opportunities  for  contagion  among  persons 
housed  in  overcrowded  quarters  is  probably  largely  responsible  for 
epidemic  outbreaks  of  the  disease.  In  1907,  the  negroes  employed 
on  the  Isthmian  Canal  and  previously  living  in  barracks  were  allowed 
to  scatter  out  along  the  line  of  the  canal,  each  man  building  his  own 
hut  and  bringing  in  his  family.     To  this  change  in  the  manner  of 

1  See  Kuhn,  Deut.  Arch.  f.  klin.  Med.,  Bd.  xxi,  p.  348,  and  Berl.  klin.  Woch.,  1879, 
p.  552. 

2  Bayrisch.  arztl.  Intelligenzbl.,  1881,  p.  424. 

3  Therapeutic  Gazette,  Detroit,  1904,  xxvi,  6. 

4  Ziemssen's  Handb.  d.  spec.  Path.  u.  Ther.,  5,  iii  Aufl.,  p.  21,  quoted  from  Frankel, 
Spec.  Path.  u.  Ther.  d.  Lungenkrankheiten,  1904,  p.  253. 

6  Quoted  from  Musser  and  Norris,  Osier.      Mod.  Med.,  vol.  ii,  p.  544. 
e  Berl.  klin.  Woch.,  April  23,  1888,  No.  17. 


'100  DISEASES  OF  THE   LUNGS 

housing  the  laborers  Gorgas1  ascribes  the  striking  coincident  drop  in 
the  mortality  from  pneumonia  noted  above. 

Individual  Factors. — (a)  Age. — Lobar  pneumonia  may  rarely  be 
congenital,  as  in  the  cases  reported  by  Levy2  and  Netter.3  In  both 
instances  the  mothers  had  pneumonia.  The  mortality  from  pneu- 
monia increases  as  age  advances,  as  shown  by  the  United  States  Census 
"  Report  for  1900,  the  death-rate  from  fifteen  to  forty  five  years  being 
100,  from  forty-five  to  sixty-five  years  263,  and  from  sixty-five  onward 
733  per  100,000  of  population.  Musser  and  Norris4  found  the  incidence 
greater  by  far  in  early  adult  life.  Of  32,681  cases,  18,813  (57  per  cent.) 
occurred  between  ten  and  forty  years.  Though  the  conclusion  is  prob- 
ably not  justified,  these  figures  suggest  that  pneumonia  is  less  frequent 
but  more  fatal  as  age  advances.  The  frequency  with  which  pneumonia 
occurs  as  a  complication  and  terminal  event  in  old  age  is  a  striking 
feature  at  postmortem  examination,  and  such  cases  may  be  classified 
under  other  causes  in  death  returns. 

(b)  Sex. — Men  are  found  to  be  more  frequently  affected  in  all  large 
series  of  cases.  Of  12,098  cases  collected  by  Musser  and  Norris, 
73  per  cent,  were  males  and  26  per  cent,  females.  According  to  their 
figures,  the  greater  frequency  among  males  does  not  seem  to  hold  for 
early  life,  and  it  seems  probable  that  the  greater  chances  for  exposure 
in  occupations  for  males  is  responsible  for  the  difference  between  the 
incidence  of  the  disease  in  the  two  sexes. 

(c)  Occupation. — Army  recruits  appear  to  be  more  susceptible  than 
hardened  soldiers.  Immigrants  are  more  likely  to  take  the  disease 
than  the  native  born.  Those  who  work  out-of-doors  are  more  fre- 
quently affected  than  those  in  indoor  vocations,  probably  because 
of  the  greater  frequency  of  exposure.  The  incidence  is  greater  among 
dwellers  in  the  city,  probably  owing  to  overcrowding  and  poor 
ventilation. 

(d)  Cold. — There  is  a  disposition  to  regard  chilling  of  the  body  as  an 
important  cause.  The  greater  frequency  of  the  disease  among  recruits 
and  immigrants  may  be  due  in  part  to  greater  susceptibility  to  changes 
of  temperature.  A  greater  incidence  of  the  disease  in  those  occupied 
out-of-doors  and  during  the  colder  months  of  the  year  suggests  that 
exposure  to  cold  may  be  a  factor.  Lipari5  obtained  a  greater  degree 
of  success  in  his  attempts  to  produce  pneumonia  in  animals  by  the 
intratracheal  injection  of  pneumonic  sputum  when  the  animals  were 
exposed  to  cold  before  or  after  the  injection.  The  explanation  is  not 
clear,  but  in  some  way  a  lower  resistance  may  be  established  by  the 
exposure.  This  subject  is  also  considered  in  the  section  on  Bronchitis. 
A  history  of  exposure  to  cold  may  be  obtained  in  a  considerable  propor- 
tion of  all  large  series  of  patients  with  pneumonia.     Of  4244  cases 

1  Loc.  cit.  2  Arch.  f.  exp.  Path.,  Bd.  xxvi,  p.  155. 

3  Compt.-rend.  d.  la  Soc.  de  Biol.,  Seance  9  mars,  1899. 

4  Osier.     Mod.  Med.,  vol.  ii,  p.  551. 
6  Lyon  med.,  October  19,  1890. 


LOBAR  PNEUMONIA  161 

collected  by  Musser  and  Norris,  755  (17  per  cent.)  gave  a  history  of 
exposure  and  "catching  cold." 

(e)  Trauma. — Litten1  divided  the  cases  into  "  traumatic  pneumonia," 
in  which  there  was  a  direct  injury  to  the  lung,  and  "contusion  pneu- 
monia," in  which  the  lung  was  injured  in  consequence  of  concussion. 
Actual  injury  to  the  pulmonary  substance  probably  occurs  in  both 
forms,  but  in  the  latter  may  take  place  without  obvious  lesion  of  the 
chest  wall.  The  site  of  the  pneumonia  does  not  always  correspond 
with  that  of  the  injury,  and  in  such  cases  contrecoup  may  be  a  factor. 
Pleural  adhesions,  pulmonary  infiltration,  emphysema  or  bronchi- 
ectasis, by  limiting  the  elasticity  of  the  lung,  may  be  predisposing 
factors.  It  is  probable  that  pneumococci  or  other  organisms  present 
in  the  respiratory  tract  find  more  favorable  conditions  for  multiplica- 
tion in  the  injured  tissue.  Not  only  croupous  but  also  broncho- 
pneumonia may  thus  arise.  Litten  observed  14  cases  (4.4  per  cent.) 
of  contusion  pneumonia  among  320  cases  of  pneumonia,  Jiirgensen2 
one  case  among  768,  and  Frankel3  7  out  of  about  830.  Miiller4  has 
recently  reviewed  the  literature. 

The  pneumonia  usually  begins  within  one  to  two  days  after  the 
injury  and  differs  from  ordinary  pneumonia  principally  in  the  hemor- 
rhagic character  of  the  sputum.  The  mortality  has  varied  in  small 
series  of  cases:  1  death  (7  per  cent.)  in  14  cases  observed  by  Litten; 
4  (28  per  cent.)  out  of  14  cases  collected  by  Stern;  and  3  (60  per  cent.) 
of  Paterson's  5  cases.  Great  variation  in  the  character  of  the  cases 
probably  accounts  for  the  difference  in  mortality.  The  combination 
of  shock  and  pneumonia  may  be  expected  to  make  the  prognosis  more 
serious  than  with  ordinary  pneumonia. 

(/)  Immersion  in  Water. — Frankel  observed  about  a  dozen  cases 
the  majority  of  which  ran  a  favorable  course.  Bein5  and  Ravenstorf6 
have  reported  instances.  The  cases  are  not  infrequent  in  hospital 
practice,  and  both  croupous  and  bronchopneumonia  may  be  observed. 
The  condition  is  probably  due  to  mechanical  injury  to  the  pulmonary 
tissue  through  the  inhalation  of  water  and  auto-infection  with  organ- 
isms already  present  in  the  tract.  Contusion  and  chilling  of  the  body 
may  also  be  factors. 

(g)  Aspiration. — This  is  more  commonly  a  cause  of  bronchopneu- 
monia and  is  considered  in  that  section. 

(h)  Inhalation. — Occupations  involving  the  inhalation  of  irritating 
gases,  steam  or  dust  may  show  a  high  incidence  of  pneumonia.  Broncho- 
is  more  frequent  than  lobar  pneumonia.    Merkel7  finds  the  incidence 

1  Zeit.  f.  klin.  Med.,  1882,  Bd.  i,  pp.  26-28. 

2  Ziemmsen's  Handb.  d.  spez.  Path.  u.  Ther.,  iii  Aufl.,  Bd.  v,  T.  i,  p.  21. 

3  Spez.  Path.  u.  Ther.  d.  Lungenkrankheiten,  p.  260. 

4  Centralb.  f.  d.  Grenzgb.  d.  Med.  u.  Chir.,  1910,  xiii,  11,  56,  93,  137,  and  187. 
6  Charite  Ann.,  1895,  xx,  150. 

6  Aerztl.  Sachverstandigenzeit.,  1906,  No.  9. 

7  Pettenkofer's  and  v.  Ziemmsen's  Handb.  d.  Hyg.  u.  Gewerbekrank.,  Abt.  4,  1882, 
III  Aufl.,  T.  ii,  p.  143. 

11 


162  DISEASES  OF   THE  LUNGS 

of  pneumonia  among  painters  7.5  per  cent.,  room  cleaners  6.9  per  cent., 
porcelain  makers  5  per  cent.,  and  cement  workers  4  per  cent. 

(i)  Personal  Condition. — Debilitating  influences  of  all  kinds  increase 
the  susceptibility  to  pneumonia.  In  this  group  is  to  be  classed 
alcoholism,  with  which  oftentimes  exposure  is  a  contributing  factor. 
Persons  suffering  from  such  chronic  diseases  as  arteriosclerosis,  val- 
vular heart  disease,  nephritis  and  malignant  disease  are  frequently 
carried  off  by  an  acute  pneumonia.  The  pneumonia  may  be  overlooked 
in  the  predominance  of  symptoms  referable  to  other  organs  than  the 
lungs. 

(j)  Relation  of  Pneumonia  to  Other  Acute  Diseases. — The  relation 
which  influenza  bears  to  pneumonia  is  difficult  to  estimate.  An  increase 
in  the  mortality  from  pneumonia  has  been  observed  during  practi- 
cally all  epidemics  of  influenza,  but  it  is  not  certain  from  the  reports 
that  such  cases  are  not  due  to  influenza  bacilli  rather  than  to  the 
pneumococcus.  Bronchopneumonia  is  far  more  common  than  lobar 
pneumonia  in  influenza,  but  the  two  forms  may  coexist  in  the  same 
case,  as  is  shown  by  autopsy.  The  pneumococcus  does  not  appear 
to  bear  any  definite  relation  to  influenza,  as  shown  by  sputum  exam- 
ination, and  on  the  other  hand  influenza  bacilli  appear  not  to  be  con- 
cerned in  typical  cases  of  lobar  pneumonia.  I  have  never  been  able 
to  demonstrate  them  in  stained  sections  of  material  from  the  lung 
in  such  cases.  In  the  cases  of  influenza  in  which  lobar  pneumonia 
occurs,  it  is  probable  that  the  respiratory  disturbances  accompanying 
influenza  favor  the  multiplication  of  pneumococci  and  determine  their 
invasion  of  the  lung. 

Typhoid  fever  and  lobar  pneumonia  may  coexist  in  rare  instances. 
Hoffmann1  found  true  lobar  pneumonia  in  18  of  250  autopsies  on 
patients  with  typhoid.  Frankel  observed  only  6  certain  or  probable 
lobar  pneumonias  due  to  the  pneumococcus  among  500  cases  of  typhoid. 
Musser  and  Xorris  found  the  two  diseases  associated  in  64  (1.4  per 
cent.)  of  4459  cases  of  pneumonia.  The  term  "typhoid  pneumonia" 
is  often  used  to  indicate  a  severe  type  of  pneumonia. 

No  definite  relation  appears  to  obtain  between  croupous  pneumonia 
and  pulmonary  tuberculosis.  A  history  of  a  typical  attack  of  croupous 
pneumonia  as  a  starting  point  for  the  disease  is  obtained  only  in  rare 
instances  in  patients  with  pulmonary  tuberculosis,  and  those  already 
subject  to  pulmonary  tuberculosis  are  not  often  attacked  by  croupous 
pneumonia.  Flick2  states  that  of  2999  cases  of  pulmonary  tuberculosis 
at  the  Phipps  Institute,  562  gave  a  history  of  pneumonia.  This  per- 
centage of  18  per  cent,  would  seem  to  contradict  the  usually  accepted 
infrequency  of  pneumonia  in  the  initiation  of  pulmonary  tuberculosis, 
but  the  pneumonic  process  referred  to  in  the  histories  may  not  have 
been  of  pneumococcal  origin.     In  the  great  majority  of  cases  of  pul- 

1  Untersuch.  iiber  <lie  path.  anat.  Veranderungen  der  Organc  b.  Abdominal  typhus, 
Leipzig,  1869;   quoted  from  Frankel. 

2  Third  Annual  Report  of  Phipps  Institute,  1907. 


LOBAR  PNEUMONIA  163 

monary  tuberculosis  in  which  a  history  of  pneumonia  is  obtained,  it 
is  probable  that  the  pulmonary  process  was  a  subacute  pulmonary 
tuberculosis  such  as  is  not  infrequently  observed,  and  may  at  first  be 
indistinguishable   from   a   non-tuberculous   infection. 

(k)  Previous  Attacks. — An  arbitrary  division  of  cases  may  be  made 
into  those  in  which  the  pneumonia  is  a  "relapse"  in  the  sense  in  which 
this  term  is  used  in  typhoid  fever,  the  pneumonia  being  observed  within 
the  period  of  convalescence,  and  those  in  which  the  disease  is  repeated 
after  a  longer  interval  of  freedom.  In  the  first  instance,  the  return 
of  the  disease  is  probably  due  to  infection  from  the  persistence  of  viru- 
lent pneumococci.  In  the  latter,  the  repetition  may  be  due  to  persist- 
ence of  the  organisms  or  reinfection  from  without.  Relapsing  'pneu- 
monia is  very  uncommon.  Wagner1  saw  only  2  instances  (0.18  per  cent.) 
of  relapse  among  1100  cases.  The  elaboration  of  protective  substances 
under  the  influence  of  the  infection  is  probably  responsible,  but  the 
duration  of  the  immunity  is  short,  and  may  actually  give  place  to  a 
condition  of  increased  susceptibility,  as  is  suggested  by  the  frequency 
with  which  later  attacks  occur.  Stortz2  found  26.4  per  cent,  of  280 
cases,  Schapira3  31.3  per  cent,  of  166  cases,  and  Morhart4  41.3  per  cent, 
of  133  cases  with  a  history  of  previous  attacks  of  pneumonia.  Several 
attacks  are  not  uncommon.  Chomel5  observed  as  many  as  ten  in  the 
same  patient,  Peter  Frank6  eleven,  and  Rush7  twenty-eight. 

Bacteriology. — In  September,  1880,  Sternberg8  found  encapsulated 
diplococci  in  the  blood  of  rabbits  after  inoculation  with  his  own  saliva. 
In  December  of  the  same  year,  Pasteur9  found  the  same  organism  in 
the  saliva  of  a  child  who  had  died  of  hydrophobia.  As  Pasteur's 
publication  is  dated  January  18,  1881,  while  Sternberg's  article  did 
not  appear  until  April,  the  priority  of  the  discovery  belongs  to  Pasteur. 

The  relation  between  the  pneumococcus  and  pneumonia  was  first 
noted  by  Eberth,10  who  found  ellipsoid  cocci  in  the  pleural,  pulmonary, 
and  pial  exudate  from  a  case  of  pneumonia  with  meningitis.  The 
importance  of  this  relation  with  pneumonia  was  not  appreciated  until 
April,  1884,  when  A.  Frankel11  found  that  it  was  the  most  frequent 
organism  occurring  in  acute  pneumonia,  and  more  carefully  described 
its  biologic  and  pathologic  character.  Weichselbaum12  later  con- 
firmed FrankeF s  observations  and  found  the  pneumococcus  94  times 

1  Die  recidivirende  Pneumonie,  Deut.  Arch.  f.  klin.  Med.,  Bd.  xlii,  p.  405. 

2  Mitt.  a.  d.  med.  klinik  z.  Wurzburg,  1885. 

3  Diss.  Wiirzburg,  1887.  4  Diss.,  Erlangen,  1892. 
6  Dictionnaire  de  medecine,  vol.  xvii,  p.  214. 

6  Interpretationes  clinicae  obs.  selec.  Tubingue,  1812,  p.  86. 

7  Cyclop,  of  pract.  med.,  vol.  iii,  p.  406. 

8  National  Board  of  Health  Report,  Washington,  April,  1881,  pp.  74-75. 

9  Bull.  Acad,  de  Med.,  Paris,  1881,  2me  ser.,  x,  379. 

10  Deut.  Arch.  f.  klin.  Med.,  Bd.  xxviii,  p.  1. 

11  Ueber  die  genuine  Pneumonie,  Kofferat,  gehalten  auf  den  III  Kongress  f.  inn.  Med., 
Wiesbaden,  1884,  p.  17;  Zeit.  f.  klin.  Med.,  Bd.  x,  p.  401;  ibid.,  Bd.  xi,  p.  437;  Deut. 
med.  Woch.,  1886,  No.  13. 

12  Wiener  med.  Jahrbucher,  neue  Folge  Jahrg.,  1886,  p.  483. 


164  DISEASES  OF  THE  LUNGS 

in  129  cases  of  lobar  pneumonia,  54  times  in  pure  culture.  As  he  found 
still  other  organisms  such  as  the  Streptococcus  pyogenes,  Friedlander's 
pneumobacillus  and  staphylococci,  he  concluded  that  genuine  lobar 
pneumonia  could  be  due  to  several  kinds  of  bacteria.  Later  observa- 
tions indicate  that  this  organism  is  to  be  regarded  as  almost  constantly 
present.  Wolff1  found  it  in  66  of  70  cases.  G.  and  F.  Klemperer2 
found  pneumococci  in  the  material  aspirated  from  the  upper  borders 
of  the  infiltration  in  all  of  15  cases  of  pneumonia.  Their  constant 
presence  was  similarly  established  by  Gamaleia.3  Weismayr4  showed 
that  pneumococci  were  the  only  organisms  present  in  the  carefully 
selected  and  washed  sputum  in  34  of  39  cases. 

Fig.  22 


Pneumococci  in  fresh  sputum. 

It  is  not  very  uncommon  to  fail  to  find  pneumococci  in  the  lungs 
of  patients  who  have  died  of  pneumonia  even  though  the  organisms 
were  abundantly  present  in  the  sputum  during  life.  In  such  cases  it 
is  probable  that  the  pneumococci  have  died  out  or  been  overgrown 
under  the  influence  of  secondary  invaders.  Secondary  invasion  by 
the  Streptococcus  pyogenes,  the  pyogenic  staphylococci,  diphtheria 
bacillus,  and  influenza  bacillus  is  not  very  uncommon.  The  typhoid 
bacillus  and  Friedlander's  pneumobacillus  are  occasionally  found. 

i  Wiener  med.  Blatter,  1887,  x,  10-14. 

2  Berl.  klin.  Woch.,  1891,  No.  35,  p.  873. 

3  Annal.  d.  l'Inst.  Past.,  T.  ii,  p.  440. 

4  Zeit.  f.  klin.  Med.,  Bd.  xxxii,  Suppl.,  p.  291. 


LOBAR  PNEUMONIA 


165 


Fig. 


The  pneumococcus  was  the  apparent  cause  in  a  large  proportion 
of  the  cases  coming  to  autopsy  at  the  Massachusetts  General  Hospital, 
but  among  192  cases,  in  23  the  infection  was  due  to  organisms  of  the 
type  of  streptococcus  mucosus  capsulatus  and  6  to  Friedlander's 
pneumobacillus. 

The  Pneumococcus  (Frankel). — Synonyms. — The  organism  is  also 
termed  the  "microbe  de  la  salive"  (Pasteur),  micrococcus  Pasteuri 
(Sternberg),  diplococcus  pneumonia?  (Weichselbaum),  and  micro- 
coccus lanceolatus. 

Morphology  and  Cultural  Peculiarities. — The  pneumococcus  is 
usually  seen  as  a  diplococcus,  the  segments  of  the  pair  being  lancet- 
shaped  with  the  broad  bases  apposed.  It  is 
occasionally  found  as  single  cocci  or  as  short 
or  even  quite  long  chains.  Staining  is  easily 
accomplished  by  the  usual  anilin  dyes  and 
by  Gram's  method.  The  organism  is  non- 
motile  and  forms  no  spores.  A  capsule  can 
usually  be  demonstrated  in  preparations 
made  from  the  sputum  or  fresh  exudates  and 
is  apparently  continuous  throughout  the 
length  of  the  chain,  with  slight  indentation 
at  the  point  of  division  of  the  segments. 
Capsules  are  usually  absent  in  cultures  on 
ordinary  media,  but  may  occasionally  be 
found  in  the  first  generation.  To  be  certain 
of  the  identity  of  the  organisms  their  cultural 
peculiarities  must  be  noted.  Growth  occurs 
on  all  ordinary  culture  media,  but  is  not 
luxuriant.  The  reaction  should  be  neutral 
or  slightly  alkaline.  Development  of  colonies 
is  most  abundant  at  37°,  but  growth  occurs 
at  a  temperature  as  low  as  24°  and  as  high 
as  42°  C.  Atypical  varieties  are  occasionally 
observed  and  difficulty  is  experienced  in 
differentiating  the  organism  from  the  strep- 
tococcus pyogenes  and  the  streptococcus 
mucosus.  On  Loffler's  blood-serum,  pneumo- 
cocci  develop  into  small,  discrete,  colorless, 

transparent  colonies.  On  agar  the"  colonies  are  small  and  transparent 
and  hardly  visible  to  the  naked  eye.  On  gelatin  after  twenty-four 
hours  the  colonies  are  small,  round,  sharply  limited,  white  or  grayish 
points  with  a  finely  granular  centre  and  more  transparent  periphery. 
The  gelatin  is  not  liquefied. 

Bouillon  is  only  slightly  clouded  and  a  fine,  white,  amorphous 
sediment  is  formed.  A  colorless  and  almost  invisible  growth 
develops  on  the  surface  of  potato.  In  milk,  there  is  acid  production 
and  coagulation  of  casein. 


Pneumococcus.  Twenty- 
four-hour  aerobic  culture  on 
blood-serum.  (.Dr.  Oscar 
Richardson.) 


166 


DfSEASES  OF  THE  H'Mis 


The  work  of  Neufeld,1  Dochez  and  Gillespie2  indicates  that  among 
the  pneumococci  are  certain  varieties  which  are  fundamentally  different, 
as  indicated  by  their  immunologic  reactions.    Dochez  and  Gillespie, 

using  two  types  of  immune  serum,  obtained  by  inoculation  of  horses 
with   two  different   strains  of  pneumococci,   found  that  white  mice 


Fig.  24 


#0  3 


•l 

I 


Pneumococcus.     Cover-glass  preparation  from  culture  on  blood-serum.      X  2000. 
(Dr.  Oscar  Richardson.) 


Fig.  25 


Streptococcus  mucosus  capsulatus  in  sputum. 

could  be  protected  against  an  otherwise  fatal  dose  of  virulent  pneu- 
mococci only  when  the  homologous  serum  was  used,  and  that  of  62 
strains  of  pneumococci,  40  (64.5  per  cent.)  were  susceptible  to  the 


1  Arb.  a.  d.  Kais.  Gesund.,  1910,  xxiv,  293. 

2  Jour.  Amer.  Med.  Assoc,  September  6,  1913. 


LOBAR  PNEUMONIA 


107 


action  of  one  or  the  other  type  of  serum  (Type  I  and  \\),  while  the 
remaining  22  strains  were  little  or  not  at  all  affected.  Of  the  22  strains, 
nine  could  be  differentiated  by  cultural  and  pathogenic  properties 
into  organisms  with  the  characters  of  the  streptococcus  or  pneumo- 
coccus  mucosus  (Type  III),  and  the  remaining  13  formed  a  hetero- 
geneous group  (Type  IV),  otherwise  indistinguishable  from  typical 
pneumococci.  Agglutinative  reactions  performed  by  mixing  equal 
quantities  of  immune  serum  and  twenty-four-hour  broth  cultures  of 
the  organisms  showed  that  the  pneumococci  could  be  identified  as 
belonging  to  one  or  the  other  of  the  two  groups  susceptible  to  the  action 
of  immune  serum  or  as  falling  outside  of  these  two  groups. 


Fig.  26 


Fig.  27 


Streptococcus  mucosus  capsulatus. 
Twenty-four-hour  aerobic  culture  on 
blood-serum.     (Dr.  Oscar  Richardson.) 


Streptococcus  mucosus  capsulatus. 
Twenty-four-hour  glucose  agar  stab  cul- 
ture.    (Dr.  Oscar  Richardson.) 


Certain  differential  features  between  the  pneumococcus  and  other 
organisms  with  which  it  is  likely  to  be  confused  may  be  noted.  The 
streptococcus  pyogenes  grows  on  Loffler's  blood-serum  in  smaller, 
drier,  and  somewhat  whiter  colonies.  On  agar  its  colonies  are  less 
transparent.  The  streptococcus  does  not  produce  acid  in  the  inulin 
medium1  of  Hiss,2  while  the  pneumococcus  does.    Streptococcus  pro- 

1  Beef-serum,  one  part;  distilled  water,  two  or  three  parts,  to  which  1  per  cent,  of 
a  5  per  cent,  solution  of  a  highly  purified  litmus  was  added.  The  medium  is  heated 
to  100°  C.  for  a  few  moments,  and  inulin  is  added  in  the  proportion  of  1  per  cent.,  after 
which  it  is  sterilized  in  the  regular  manner  on  three  successive  days. 

2  Jour.  Exp.  Med.,  1905,  vol.  vii,  No.  5. 


1 68 


DISEASES  OF  THE  LUNGS 


duces  a  precipitate  in  glucose-serum-agar1  while  the  pneumococcus  only 
rarely  does  so.  The  streptococcus  is  resistant  against  bile,2  and  the 
pneumococcus  is  dissolved  as  noted  by  Neufeld.3 

The  streptococcus  mucosus  capsulatus  has  distinctive  growth  char- 
acteristics and  usually  presents  a  more  abundant,  usually  confluent, 
smooth,  watery  layer  on  the  surface  of  blood-serum.  Stab  cultures  in 
glneose-agar-agar  of  a  reaction  of  plus  0.5  to  pins  1.0  after  twenty- 
four  hours  in  the  incubator  present  a  grayish,  translucent  band  of 
growth  along  the  needle  track  as  pointed  out  by  Richardson.4  Toward 
the  middle  and  deeper  parts  of  the  tube  this  band  widens  out  into  oval 
form  in  one  plane  to  three  to  four  times  the  width  of  the  intervening 

Fig.  2S 


•'  •   4 

®' 

1        V 

•i  i 

•*     4: 

»                                   • 

0    ■ 
k 

& 

Z/ 
>• 

• 

-y 

\  f.9 

''s 

■.    ii«: 

It) 

•S 

ml 

Streptococcus  mucosus  capsulatus.     Cover-glass  preparation  from  culture  on  blood- 
serum.      X  2000.      (Dr.  Oscar  Richardson.) 


growth.  The  streptococcus  mucosus  ferments  inulin,  throws  out  a 
precipitate  in  glucose-serum-agar,  and  is  dissolved  by  bile.  Accord- 
ing to  Libman,  the  streptococcus  grows  on  blood-plates  (made  from 
human  or  ox  blood)  in  colonies  which  show  a  definite  large  (2  to  3 
mm.)  perfectly  clear  zone  about  them  which  should  persist  in  several 
generations.     Pneumococci  produce  a  green  color. 

1  0.5  per  cent,  glucose  is  used  and  an  ascitic  serum  having  a  specific  gravity  of  1015 
or  more.  Libman,  Jour.  Med.  Research,  1901,  i,  89,  also  Trans.  Assoc.  Amer.  Phys., 
1910,  vol.  xxv. 

2  This  test  may  be  performed  by  mixing  1  c.c.  of  a  twenty-four-hour  culture  of  pneu- 
mococci with  1  c.c.  of  a  freshly  prepared  solution  of  Merck's  taurocholate  of  soda  and 
shaking  well. 

3  Zeit.  f.  Hyg.  u.  Infektionskr.,  1900,  xxxiv,  454. 

4  Jour.  Med.  Research,  May  23  and  June  4,  1901,  vol.  v,  No.  11. 


LOBAR  PNEUMONIA  169 

The  relation  whieh  the  streptocoecus  and  the  streptococcus  mucosus 
capsulatus  bear  to  the  pneumococcus  cannot  yet  be  regarded  as  settled, 
and  it  may  be  that  closely  related  organisms  of  the  streptoeoccus- 
pneumococcus  group  are  modified  pneumococci. 

Rosenow1  has  succeeded  in  changing  different  strains  of  the  strepto- 
coccus group  (hemolytic  streptococcus,  streptococcus  viridans,  strepto- 
coccus mucosus)  each  one  into  the  others  and  into  pneumococci, 
and  pneumococci  into  streptococci,  and  back  again  into  pneumococci. 
Transformation  of  some  of  the  strains  was  complete,  as  indicated  by 
a  study  of  morphology,  capsule  formation,  fermentative  powers, 
solubility  or  insolubility  in  bile  and  NaCl  solution,  behavior  toward 
the  respective  broth-culture  filtrates  (Marmorek's  test),  production 
of  opsonin,  agglutination  by  antipneumococcus  and  antistreptococcus 
serum  and  the  more  or  less  specific  pathogenic  powers. 

Fig.  29 


Streptococcus  mucosus  capsulatus  in  pneumonic  exudate.      X  1500. 
(Dr.  Oscar  Richardson.) 

Pneumococci  in  Apparently  Healthy  Individuals. — The  results  of 
various  observers  working  under  the  Medical  Commission  for  the 
Investigation  of  Acute  Respiratory  Diseases,  of  the  Department  of 
Health  of  the  City  of  New  York,2  show  that  pneumococci  can  be 
recovered  from  about  one-half  the  number  of  cases  in  which  the  saliva 
of  apparently  healthy  persons  is  examined.  The  experience  of  Hiss3 
is  even  more  striking.    Of  15  persons  from  each  of  whom  one  specimen 

1  Jour.  Infect.  Dis.,  January,  1914. 

2  Jour.  Exp.  Med.,  1905,  vol.  vii,  No.  5.  3  Ibid. 


170  DISEASES  OF  THE  LUNGS 

of  sputum  was  examined,  typical  pneumococci  were  found  in  7  (4(> 
per  cent.)  by  mouse  inoculation.  In  the  remaining  7  cases,1  repeated 
tests  of  the  saliva  were  made,  and  in  these  eases  typical  pneumococci 

were  found  in  (»  (85  per  cent.).  Atypical  and  avirulent  strains  are  more 
common  in  the' healthy  mouth  than  in  the  sputum  of  patients  with  or 
convalescent  from  pneumonia.  Residence  in  the  city  or  country 
and  indoor  or  outdoor  occupations  apparently  play  little  part  in  the 
frequency.  Longcope  and  Fox2  found  the  percentage  of  the  true 
pneumococcus  type  not  very  high  in  November,  an  enormous  increase 
in  December  and  January,  and  a  gradual  fall  to  a  1owt  level  in  March 
and  April.  A  larger  proportion  of  persons  who  come  in  contact  with 
patients  with  pneumonia  harbor  the  pneumococcus  than  of  persons 
not  so  exposed.  Convalescents  from  pneumonia  may  carry  virulent 
organisms  in  the  respiratory  passages  for  weeks  or  months. 

Pneumococci  Outside  the  Body. — The  viability  of  the  pneumococcus 
outside  the  body  is  short,  and  cultures  die  out  rapidly  unless  carefully 
attended.  Transplants  must  be  made  every  two  to  three  days.  Occa- 
sional passage  through  animals  may  be  necessary  for  the  maintenance 
of  the  strain.  It  is  resistant  against  cold,  but  killed  in  the  moist  state 
by  exposure  to  a  temperature  of  52°  for  ten  minutes.  Ordinary  dis- 
infectants are  quickly  effective.  In  sputum,  the  organism  is  resistant 
to  a  considerable  degree.  Wood3  found  that  in  moist  sputum  pre- 
served in  the  dark  at  room  temperature,  the  average  life  of  the  pneu- 
mococcus was  with  considerable  variation  eleven  days;  at  0°  C.  thirty- 
five  days;  and  at  room  temperature  in  a  strong  light  less  than  five 
days.  In  dried  sputum  in  the  dark,  the  organism  was  found  to  live 
on  an  average  for  thirty-five  days;  in  diffuse  light  thirty  days;  and  in 
sunlight  less  than  four  hours.  In  powdered  sputum,  even  in  the  dark, 
death  occurred  in  from  one  to  four  hours;  under  exposure  to  sunlight 
within  an  hour.  On  cloth  the  life  of  the  organism  wTas  somewhat 
longer  than  on  a  non-absorbing  surface.  Sprayed  sputum  particles 
remained  in  suspension  twenty-four  hours,  but  all  masses  of  a  size 
sufficient  to  contain  bacteria,  settled  at  the  rate  of  about  40  cm.  per 
hour.  When  sputum  containing  pneumococci  is  sprayed,  the  organisms 
rarely  survived  for  more  than  an  hour  and  often  died  in  less  time. 
Under  exposure  to  sunlight  while  in  suspension,  pneumococci  in  spray 
are  destroyed  within  a  half-hour. 

Toxin  Production. — Attempts  to  demonstrate  a  soluble  toxin  in 
pneumococcus  cultures  have  usually  failed,  and  the  organism  does  not 
apparently  produce  such  a  substance  in  fluid  media.  The  toxin  is 
probably  intracellular  and  set  free  within  the  body  in  the  course  of 
infection  by  destruction  of  the  organisms.  In  support  of  this,  Rosenow4 
and  Cole5  have  found  that  the  peritoneal  exudates  obtained  by  infect- 
ing animals  with  pneumococci  are  toxic.     Cole  has  also  shown  that 

1  So  stated  in  text,  ibid.,  p.  576.     .    2  Ibid.,  p.  449.        3  Ibid.,  p.  623. 
4  Jour.  Infect.  Dis.,  1912,  xi,  94.         6  Jour.  Exp.  Med.,  1912,  xvi,  644. 


LOBAR  PNEUMONIA.  171 

when  pneumococci  are  dissolved  in  dilute  solution  of  bile  salts  and  the 
resulting  solution  is  injected  intravenously  into  guinea-pigs  and  rabbits, 
these  animals  very  constantly  show  the  same  symptoms  seen  in  acute 
anaphylaxis.     The  toxin  is  hemolytic  for  red  blood  corpuscles.3 

Immunity. — In  comparison  with  ordinary  laboratory  animals  used 
for  experimentation,  man  appears  to  be  relatively  insusceptible  to 
infection  with  the  pneumococcus,  as  indicated  by  the  less  common 
occurrence  of  rapidly  fatal  septicemia  without  marked  local  reaction. 
The  degree  of  natural  immunity  probably  varies  in  different  indi- 
viduals, but  its  importance  is  difficult  to  estimate  in  the  face  of  wide 
variations  in  virulence  of  the  infecting  organisms.  Little  or  no 
evidence  can  be  presented  in  favor  of  the  acquisition  of  any  consider- 
able or  lasting  protection  against  subsequent  infection  by  the  recovery 
from  an  attack  of  pneumonia.  In  fact,  the  frequency  of  recurrence 
of  pneumonia  is  one  of  its  most  striking  features,  and  one  attack  seems 
rather  to  predispose  than  to  protect  against  later  infection.  Recent 
researches  on  man  and  on  animals  are  hopeful,  however,  in  that  they 
suggest  that  a  limited  and  transient  immunity  may  be  acquired. 
Rabbits  can  be  immunized  against  infection  with  pneumococci  in 
various  ways.  Filtrates  of  cultures  or  dead,  attenuated  or  small 
doses  of  virulent  cultures  have  been  successfully  used.  The  process 
of  immunization  is  probably  best  accomplished,  however,  by  gradually 
increasing  intravenous  doses  of  virulent  organisms  as  described  by 
Neufeld.2  Susceptible  animals  can  thus  be  protected  against  many 
times  the  otherwise  fatal  dose  of  virulent  pneumococci,  and  the  serum 
of  an  animal  so  immunized  is  capable  of  preventive  and  limited  curative 
action  against  pneumococcus  infection.  Neufeld  and  Haendel3  have 
obtained  serum  from  immunized  horses  and  donkeys  which  will  protect 
against  the  100,000-  to  1,000,000-fold  fatal  dose.  Antipneumococcus 
serum  appears  to  be  potent  against  typical  strains  of  pneumococci, 
but  not  for  all.  Against  atypical  strains,  according  to  Neufeld  and 
Haendel,4  ordinary  immune  serum  is  ineffective,  and  inasmuch  as 
such  strains  may  be  a  cause  of  pneumonia,  a  determination  of  the  type 
of  organism  is  desirable  in  any  given  case. 

Investigations  have  been  made  for  the  purpose  of  demonstrating 
protective  substances  in  man,  and  more  especially  in  connection  with 
the  crisis  in  pneumonia,  the  striking  features  of  which  would  suggest  that 
at  this  period  in  the  course  of  the  disease  such  substances  might  be 
demonstrable.  The  results  are  not  wholly  in  accord,  but  in  general 
indicate  that  protective  substances  of  a  bacteriotropic  nature  are 
present.  In  1891,  G.  and  F.  Klemperer5  found  that  the  blood  of  patients 
who  had  recovered  from  an  attack  of  pneumonia  would  protect  rabbits 

i  Cole.      Jour.  Exp.  Med.,  1914,  xx,  346. 

2  Zeit.  f.  Hyg.,  1902,  Bd.  xl,  p.  68;  ibid.,  1900,  Bd.  xxxiv,  p.  457;  also  Zeit.  f.  Irnmuni- 
tatsforsch.,  1903,  I  Th.,  3,  orig.,  p.  159. 

3  Zeit.  f.  Immunitatsforsch.,  1909,  I  Th.,  3,  orig.,  p.  159. 

4  Arb.  a.  d.  k.  Gesundheitsamte,  1910,  xxxiv,  293. 
^  Berl.  klin.  Woch.,  1891,  xxviii,  833,  869. 


172  DISEASES  OF  THE  LUNGS 

against  infection  with  the  pneumococcus.  Neufeld  and  Haendel1 
also  found  that  the  serum  of  convalescents,  as  a  rule  but  not  constantly, 
contained  protective  substances  in  variable  amount.  Seligmann  and 
Klopstock,-  Boettcher,3  and  Strouse4  failed  to  confirm  these  observa- 
tions. Xeufeld'  and  Haendel5  offer  an  explanation  of  the  negative 
results  obtained  by  Seligmann  and  Klopstock  and  Boettcher  in  the 
employment  of  a  different  teclmic,  and  in  this  article  report  the 
successful  demonstration  of  protective  substances  in  every  case. 
Dochez6  finds  protective  substances  usually  present  in  the  blood  of 
patients  recovering  from  pneumonia.  Their  appearance  as  a  rule 
coincides  rather  sharply  with  the  period  of  critical  fall  of  the  tempera- 
ture and  the  disappearance  of  symptoms.  An  important  matter  in 
their  recognition  appears  to  be  the  use  both  of  pneumococci  and  serum 
from  the  same  patient. 

The  character  of  the  protective  substance  in  antipneumococcus 
serum  cannot  yet  be  regarded  as  settled.  Toxin  is  not  found  in  fluid 
media  in  which  pneumococci  are  grown,  but  the  success  of  Ilosenow 
and  Cole  in  demonstrating  toxin  in  peritoneal  exudates  suggests 
that  an  endotoxin  may  be  responsible,  against  which  it  is  unsafe  to 
assume  that  the  body  fails  to  produce  antitoxin.  Lysis  of  pneumo- 
cocci has  been  noted  by  Neufeld,7  Wadsworth8  and  others  in  the  hang- 
ing drop  of  serum  from  a  highly  immunized  animal.  It  appears  to  be 
slight  when  tested  in  this  way  in  comparison  with  that  obtained  in  a 
similar  manner  with  the  organisms  of  cholera  or  typhoid  fever.  The 
protective  substances  in  immune  serum  are  more  generally  ascribed 
to  their  content  of  bacteriotropine  or  opsonin  which  is  thought  to  act 
on  the  bacteria  and  favor  their  ingestion  and  destruction  by  phago- 
cytes. Attempts  to  demonstrate  these  substances  in  vitro  are  subject 
to  great  technical  difficulties,  and  some  doubt  must  be  entertained 
concerning  conclusions  drawn  from  such  studies. 

A  consideration  of  the  results  thus  far  obtained  in  the  study  of 
immunity  in  its  relation  to  pneumococcus  infections,  suggests  that 
recovery  from  pneumonia  cannot  be  wholly  ascribed  to  the  production 
of  protective  substances  in  the  blood,  however  important  they  may 
be  as  a  partial  solution  of  the  problem.  Antipneumococcus  serum 
is  apparently  capable  of  only  limited  curative  action  in  experimental 
infections  and  has  as  yet  not  been  shown  to  be  strikingly  effective  in 
man ;  protective  substances  in  the  blood-serum  of  patients  after  recovery 
are  neither  constantly  nor  decisively  demonstrable,  and  recovery 
from  pneumonia  fails  to  confer  any  considerable  or  lasting  protection 
against  subsequent  attacks.  On  the  other  hand,  in  pneumonia  as  in 
no  other  disease,  the  fight  between  host  and  parasite  is  not  only  fierce, 

i  Zeit.  f.  Immunitatsforsch.,  1909,  I  Th.,  3,  p.  1G8.       2  Ibid.,  1909-10,  orig.,  iv,  103. 

3  Deut.  Arch.  f.  klin.  Med.,  1909-10,  xcviii,  93. 

4  Jour.  Exp.  Med.,  1911,  xiv,  109. 

6  Arb.  a.  d.  k.  Gesundheitsamte,  1910,  xxxiv,  16G. 

6  Jour.  Exp.  Med.,  1912,  xvi,  665.  7  Zeit.  f.  Hyg.,  1902,  xl,  54. 

s  Jour.  Exp.  Med.,  1912,  p.  16. 


LOBAR  PNEUMONIA  173 

but  ends  decisively  in  favor  of  one  or  the  other  combatants,  and  it 
seems  fair  to  expect  that  the  defensive  mechanism  will  when  discovered 
be  more  obviously  apparent.  The  most  striking  features  of  pneumonia, 
are  the  crisis  and  the  rapid  and  complete  resolution  of  the  affected 
lung.  The  pulmonary  tissue  seems  to  be  the  chief  seat  of  the  struggle, 
and  it  is  not  unnatural  to  expect  that  study  of  the  lung  itself  may 
lead  to  more  definite  results. 

Welch1  in  1890  observed  that  lysis  of  pneumococci  within  their 
capsules  could  be  demonstrated  under  the  microscope  during  resolu- 
tion of  the  pneumonic  exudate.  The  nature  and  the  source  of  the 
substance  leading  to  dissolution  of  the  organisms  is  not  known,  but 
various  experimenters  have  shown  that  leukocytes  yield  substances 
capable  of  destroying  bacteria  and  splitting  protein,  and  it  may  be 
that  a  substance  derived  from  the  leukocytes  is  responsible  for  the 
local  changes  observed  in  resolution  in  pneumonia.  Flexner2  calls 
attention  to  this  aspect  of  the  defenses  against  pneumonia,  and  Lamar3 
and  Jobling  and  Strouse4  report  suggestive  experiments,  the  exact 
bearing  of  which  on  this  problem  cannot  yet  be  regarded  as  settled. 

Pneumococci  in  Non-pulmonary  Lesions.  —  Direct  extension  of  the 
pneumococci  is  responsible  for  the  practically  constant  occurrence 
of  pleuritis  as  a  complication  of  lobar  pneumonia.  Pericarditis  may 
likewise  arise.  Secondary  lesions  elsewhere  may  be  due  to  passage 
along  the  lymphatics  or  invasion  of  the  blood-stream.  In  certain 
cases,  the  passage  of  pneumococci  through  the  lymphatics  may  be 
successfully  blocked  by  the  lymph  nodes.  In  others,  the  barrier  offered 
by  the  glands  may  be  passed  and  the  organisms  thus  reach  the  blood- 
stream. Direct  invasion  of  injured  bloodvessels  may  be  the  method 
of  entry  to  the  blood-stream.  Septicemia  complicating  lobar  pneu- 
monia is  usually  unassociated  with  localizing  lesions  in  other  parts  of 
the  body,  but  endocarditis,  meningitis,  peritonitis,  otitis  media,  and 
other  processes  may  be  observed.  Pneumococci  alone  or  mixed 
with  other  organisms  may  be  responsible  for  bronchitis,  tonsillitis, 
rhinitis,  etc.  In  some  instances  complicating  lesions  are  due  to  other 
organisms  than  the  pneumococcus.  The  pneumococcus  is  not  infre- 
quently a  cause  of  infection  in  various  parts  of  the  body  in  the  absence 
of  a  primary  lesion  in  the  lung.  Mixed  infections  are  not  uncommon 
in  such  instances. 

Pneumococcus  Septicemia. — Investigations  show  that  pneumococci 
can  be  demonstrated  in  the  blood  in  a  large  proportion  of  the  cases. 
Prochaska5  obtained  diplococci  from  the  blood  in  all  (100  per  cent.) 
of  50  cases.    Rosenow's6  cultures  were  positive  in  160  (91  per  cent.)  of 

1  Johns  Hopkins  Hosp.  Bull.,  1890,  i,  73.  2  Jour.  Exp.  Med.,  1911,  xiii,  1. 

3  Ibid.,  pp.  6  and  380.  4  Ibid.,  1912,  xvi,  269. 

6  Bakteriologische  Blutuntersuchungen  bei  Pneumonien,  Cent.  f.  inn.  Med.,  1900, 
xxi,  1145,  and  Untersuchungen  iiber  die  Anwesenheit  von  Microorganismen  ini  Blute 
bei  den  Pneumoniekranken,  Arch.  f.  klin.  Med.,  1901,  lxx,  559. 

6  Studies  in  Pneumonia  and  Pneumococcus  Infections,  Jour.  Infect.  Dis.,  1904,  i,  280, 
and  The  Blood  in  Lobar  Pneumonia,  Jour.  Amer.  Med.  Assoc,  1905,  xliv,  871. 


174  DISEASES  OF   THE   LUNGS 

17.")  cases.  Others  have  demonstrated  the  organism  in  a  smaller  pro- 
portion, Schottmiiller1  in  23  per  cent,  of  209  eases,  Cole2  in  30  per  cent, 
of  30  cases,  Wiens3  in  79  per  cent,  of  33  cases,  Strouse  and  Clough4  in 
56  per  cent,  of  25  eases,  and  Dochez5  in  18  (50  per  cent.)  of  37  eases. 
The  organisms  may  he  obtained  from  the  hlood  before  the  physical 
signs  of  pneumonia  are  present,  and  occasionally  as  long  as  two  to 
three  days  after  the  temperature  has  fallen  to  normal,  hut  positive 
cultures  are  less  often  obtained  as  the  crisis  is  approached,  from  patients 
who  recover,  hence  a  persistent  septicemia  in  general  may  be  regarded 
as  relatively  unfavorable.  Positive  cultures  are  most  constant  when 
large  amounts  of  blood  (10  to  20  c.c.)  are  taken.  The  blood  should 
be  diluted  at  once  with  50  to  75  parts  of  nutrient  broth  in  flasks. 
As  soon  as  growths  appear  in  the  flasks,  transplants  may  be  made  to 
solid  media.  Pneumococci  were  demonstrated  in  the  heart's  blood 
in  42  of  152  cases  at  autopsy  at  the  Massachusetts  General  Hospital. 
They  are  not  infrequently  found  in  the  blood  at  autopsy  in  cases  with- 
out distinct  localization  in  the  lung.  In  most  cases  death  in  pneu- 
monia is  probably  due  to  septicemia.  Frankel6  reports  a  case  in  which 
by  blood-culture  during  life,  2700  colonies  of  pneumococci  per  cubic 
centimeter  of  blood  were  found.  Dochez  found  10,000  in  one  case  on 
the  fourth  day,  and  65,000  at  the  time  of  death  in  another. 

Animal  Experimentation. — The  pneumococcus  is  pathogenic  for 
various  animals,  but  presents  -considerable  variation  in  virulence. 
The  rabbit  and  mouse  are  most  susceptible,  the  guinea-pig,  dog,  sheep 
and  rat  less  susceptible,  and  the  pigeon  is  immune.  The  type  of  infec- 
tion in  animals,  however,  differs  from  that  in  man  in  the  production 
of  relatively  slight  local  reaction  and  usually  marked  general  septi- 
cemia. At  the  point  of  inoculation  there  is  a  slight  fibrinous  inflam- 
mation. The  spleen  is  usually  enlarged  and  soft  and  large  numbers 
of  pneumococci  are  found  in  the  blood.  If  less  virulent  cultures  are 
used  or  the  injections  are  made  into  less  susceptible  animals,  the  local 
lesion  becomes  more  and  the  general  infection  less  marked. 

Numerous  attempts  by  different  methods  have  been  made  to  induce 
pneumonia  in  animals  with  varying  but  usually  negative  results. 
Systemic  infection,  either  by  subcutaneous  or  intravenous  injection 
of  cultures,  has  constantly  failed.  The  exceptional  success  of  Gamaleia7 
in  the  constant  production  of  pneumonic  lesions  in  dogs  and  sheep 
by  intrathoracic  injection  of  cultures,  and  of  Tchistovitch8  in  7  of 
19  intratracheal  injections  in  cats,  failed  of  confirmation  by  later 
observers.    Wadsworth9  reviews  the  literature  and  records  in  his  own 

1  Munch,  med.  Woch.,  1905,  lii,  1425. 

2  Johns  Hopkins  Hosp.  Bull.,  1902,  xiii,  130. 
s  Zeit.  f.  klin.  Med.,  1908,  Ixv,  53. 

4  Johns  Hopkins  Hosp.  Bull.,  August,  1910. 

s  Jour.  Exp.  Med.,  1912,  xvi,  680. 

r'  Internal  Beitnige  z.  inn.  Med.,  1902,  ii,  103. 

7  Ann.  do  l'lnst.  Past.,  1888,  ii,  440. 

8  Ibid.,  1890,  iii,  285. 

9  Amer.  Jour.  Med.  Sci.,  1904,  cxxvii,  851. 


LOBAR  PNEUMONIA  175 

work  a  greater  measure  of  success  than  had  previously  been  obtained 
by  most'  investigators.  A  high  degree  of  virulence  in  the  organisms 
used  for  the  experimentation  in  susceptible  animals  often  leads  to 
fatal  septicemia  without  the  production  of  local  pulmonary  lesions. 
In  his  experiments,  11  rabbits,  rendered  less  susceptible  by  preliminary 
immunization,  were  tracheally  injected  with  1  c.c.  of  a  highly  virulent 
culture  of  pneumococci  grown  in  normal  rabbits'  serum  diluted  with 
broth.    All  showed  pneumonia  at  autopsy. 

Lamar  and  Meltzer1  have  obtained  the  most  striking  success  hitherto 
reported.  Dogs  were  infected  by  the  injection  of  pure  cultures  of  the 
pneumococcus  through  a  catheter  or  small  stomach-tube  introduced 
into  a  bronchus  by  the  insufflation  method  of  Meltzer  and  Auer.2 
Of  44  animals  dying  or  killed  within  twelve  days  of  inoculation,  42 
were  found  to  have  pneumonia.  In  the  remaining  2  the  lung  was 
normal.  The  failure  in  these  two  instances  was  ascribed  to  introduc- 
tion of  the  tube  into  the  esophagus  rather  than  the  larynx.  The 
mortality  was  at  least  16  per  cent.  The  fatal  cases  closely  resembled 
lobar  pneumonia  in  man.  The  non-fatal  cases  ran  a  milder  and  shorter 
course.  The  amount  of  the  culture  injected  seemed  to  influence  the 
result,  larger  quantities  having  been  injected  in  the  fatal  cases.  Varia- 
tion in  resistance  of  the  animals  was  not  noted.  Success  seemed  to  be 
due  to  obliteration  of  a  large  number  of  bronchi  by  the  culture,  thus 
affording  a  favorable  opportunity  for  the  growth  of  the  organisms  and 
the  production  of  the  local  lesion. 

That  pneumonia  of  a  lobar  type  is  a  special  feature  of  pulmonary 
infection  with  pneumococci  is  suggested  by  the  experiments  of  Woll- 
stein  and  Meltzer3  who  found  that  intrabronchial  insufflation  of  pure 
cultures  of  the  streptococcus  or  the  influenza  bacillus  produced  broncho- 
and  not  lobar  pneumonia.  The  differences  in  the  nature  of  the  lesion 
seem  to  be  due  to  differences  in  the  species  rather  than  to  the  degree 
of  virulence  of  the  infecting  organisms,  since  non-virulent  pneumococci 
cause  the  development  of  a  lesion  with  the  gross  appearances  of  lobar 
pneumonia  and  an  exudate  in  the  lung  which  in  general  leaves  the 
framework  unaffected,  as  shown  by  Wollstein  and  Meltzer.4  But  the 
pneumonia  produced  by  non-virulent  pneumococci  tends  to  undergo 
a  more  rapid  resolution,  the  disease  is  non-fatal,  the  blood  is  not  invaded 
by  the  organisms,  and  the  exudate  is  strikingly  poor  in  fibrin. 

The  influence  of  leukocytosis  in  increasing  the  resistance  of  animals 
to  pneumococcus  infection  is  suggested  by  the  work  of  Winternitz 
and  Hirschfelder5  and  Kline  and  Winternitz.6  Pneumonia  was  pro- 
duced by  the  insufflation  method  of  Lamar  and  Meltzer  in  rabbits 
previously  rendered  aplastic  by  the  injection  of  benzol.  In  eight 
animals  thus  treated,   the  resistance  to  pneumonia  was  markedly 

1  Proc.  Soc.  Exp.  Biol,  and  Med.,  1909-10,  vii,  102;    Jour.  Exp.  Med.,  1912,  xv,  133. 

2  Med.  Rec.,  1910,  lxxvii,  477,  and  Jour.  Amer.  Med.  Assoc.,  1911,  lvii,  521. 

3  Jour.  Exp.  Med.,  1912,  xvi,  126.  *  Ibid.,  1913,  xvii,  353. 
B  Ibid.,  1913,  xvii,  657.                                                                   «  Ibid.,  1913,  xviii,  50. 


176  DISEASES  OF  THE  LUNGS 

reduced  and  there  seemed  to  be  a  striking  overgrowth  of  pnenmococci 
in  the  lungs.  On  the  other  hand,  animals  treated  with  toluol,  a  similar 
chemical  compound  causing  no  leukopenia,  showed  no  diminished 
resistance.  The  production  of  leukocytosis  by  the  repeated  injection 
of  toluene  or  protein  substances  appeared  to  increase  the  resistance 
of  the  infected  animals. 

Pathogenesis. — It  has  been  established  that  a  large  proportion  of 
apparently  healthy  individuals  act  as  host  for  virulent  pneumococci, 
but  it  is  not  as  yet  clear  how  the  pulmonary  infection  occurs.  Primary 
invasion  of  the  blood  or  the  bronchial  glands  and  secondary  localiza- 
tion in  the  lung  have  been  suggested  in  explanation.  The  constant 
failure  to  produce  pneumonia  in  animals  by  intravenous  injection  is 
against  the  hematogenous  theory.  Aspiration  of  infected  material 
from  the  mouth  seems  the  most  likely  explanation.  A  very  consider- 
able proportion  of  patients  with  pneumonia  give  the  history  of  a  pre- 
ceding acute  respiratory  infection.  Such  predisposing  factors  as  a 
chill  or  trauma,  increased  virulence  of  the  organisms  or  lowered  resist- 
ance of  the  patient  may  be  of  importance.  The  inhalation  theory  is 
materially  supported  by  the  finding  at  autopsy  of  the  disease  in  its 
more  advanced  stages  in  the  central  parts  of  the  lung  and  the  successful 
insufflation  experiments  of  Lamar  and  Meltzer.  Obliteration  of  the 
lumen  of  the  bronchi  by  a  fibrinous  exudate  caused  by  the  pneumo- 
coccus  may  be  an  important  determining  factor  in  the  lobar  character 
of  the  pneumococcus  infection.  The  varying  response  of  animals  to 
infection  with  the  pneumococcus  suggests  that  the  relative  insuscepti- 
bility of  man  and  infection  with  organisms  of  high  virulence  also 
play  a  part  in  the  localization  of  the  infection  in  the  lung. 

Metabolism. — Atwater  and  Langworthy,1  in  a  summary  of  27  cases, 
found  that  the  assimilation  of  the  nitrogenous  constituent  of  the  food 
was  poorer  during  the  febrile  period  than  in  convalescence,  and  that 
a  greater  destruction  of  tissue  protein  took  place  during  the  febrile 
period  and  in  two  or  more  days  of  convalescence.  A  portion  of  the  nitro- 
gen of  the  food  was  retained  during  a  part  of  convalescence  when  the 
patient  began  to  take  sufficient  food.  The  increased  output  of  nitrogen 
in  the  urine  in  the  period  immediately  after  the  crisis  may  be  chiefly 
accounted  for  by  the  intensified  destruction  of  proteid  tissue.  The 
ratio  of  the  extractives  to  uric  acid  and  urea  was  higher  than  normal 
in  all  cases  in  the  fever  period  and  in  the  majority  of  cases  during 
convalescence. 

H.  W.  Cook2  studied  the  nitrogen  excretion  in  pneumonia  and  its 
relation  to  resolution.  Determinations  of  the  total  nitrogen  in  the 
urine  by  the  Kjeldahl  method  were  made  on  22  cases.  He  found  that 
in  most  cases  more  nitrogen  was  excreted  during  the  days  of  resolu- 
tion than  would  correspond  to  the  original  quantity  of  exudate  poured 

1  A  Digest  of  Metabolism,  Experiments,  etc.,  Bulletin  No.  45,  Office  of  Experiment 
Stations,  United  States  Department  of  Agriculture,  1898,  p.  241. 

2  Johns  Hopkins  Hosp.  Bull.,  December,   1902. 


LOBAR   PNEUMONIA  177 

out  into  the  involved  lung.  He  regards  the  excess  of  nitrogen  excreted 
as  representing  in  great  part  a  continuation  of  the  formation  and  an 
absorption  of  inflammatory  exudation  plus  other  tissue  destruction. 
In  cases  in  which  there  is  a  marked  delay  in  resolution,  he  believes 
that  the  continued  high  output  of  nitrogen  indicates  a  continuation 
of  the  local  inflammatory  process.  In  rapid  resolution  the  leukocytosis 
curve  follows  the  nitrogen  curve  with  a  very  striking  parallelism  and 
seems  to  point  to  a  causal  relation  between  leukocytes  and  resolution. 

Wolf  and  Lambert1  studied  the  nitrogen  and  sulphur  metabolism 
in  19  cases  of  pneumonia  of  varying  degrees  of  severity.  They  found 
that  the  cases  of  milder  type  show  a  smaller  loss  in  nitrogen  and  sul- 
phur than  those  of  a  more  severe  grade.  The  daily  loss  in  nitrogen  on 
a  diet  adequate  to  protect  a  resting  individual  from  nitrogen  loss  may 
be  from  20  to  25  grams.  The  relative  desamidating  capacity,  as  shown 
by  the  ratio  of  urea  to  total  nitrogen,  is  comparable  to  that  of  a  normal 
subject.  The  capacity  for  the  oxidation  of  the  cystin  group,  as  exhibited 
by  the  ratio  of  total  sulphate  sulphur  to  total  sulphur,  is  quite  as  high, 
if  not  higher  than  normal.  During  the  period  of  hyperpyrexia,  exces- 
sive amounts  of  creatinin  are  eliminated,  and  this  is  followed  during 
convalescence  by  a  subnormal  excretion  of  creatinin.  This  is  taken 
to  indicate  the  endeavor  on  the  part  of  the  organism  to  repair  the  losses 
sustained  during  the  height  of  the  toxemia.  In  the  severe  cases  of 
pneumonia,  large  amounts  of  creatin  are  also  excreted.  This  is  seen 
particularly  during  the  time  of  greatest  nitrogen  loss.  During  con- 
valescence the  creatin  disappears  from  the  urine.  In  some  of  the  lethal 
cases  the  amount  of  creatin  excreted  on  the  day  terminating  the  ill- 
ness is  as  high  as  the  amount  of  creatinin  excreted.  During  hyper- 
pyrexia, especially  in  cases  severely  toxic  in  type,  unusually  high 
amounts  of  undetermined  nitrogen  are  excreted.  The  sulphur  excre- 
tion runs  more  or  less  parallel  with  that  of  the  nitrogen,  but  it  appears 
that  in  some  of  the  cases  the  catabolism  of  proteins  rich  in  sulphur 
is  not  so  marked  as  those  in  which  the  content  of  sulphur  is  small. 

Oxygen  Content  of  Blood. — Butterfield  and  Peabody2  found  a  reduc- 
tion of  oxygen  capacity  below  the  normal  level  without  a  corresponding 
diminution  of  hemoglobin  in  some  cases  of  pneumonia  (Peabody), 
and  in  guinea-pigs  and  rabbits  with  pneumococcus  infection.  It  was 
also  found  that  a  definite  drop  in  the  oxygen  capacity  was  constantly 
produced  by  the  action  of  pneumococcus  cultures  on  washed  rabbit 
red -blood  corpuscles  in  vitro,  and  that  this  was  due  to  the  formation  of 
methemoglobin  (or  some  derivative  of  hemoglobin  with  identical 
optical  constants  for  three  regions  in  the  spectrum) .  In  rabbits  injected 
intravenously  with  sufficiently  large  doses  of  pneumococci  to  produce 
a  severe  bacteriemia,  Peabody3  noted  polypnea,  cyanosis  of  the  mucous 
membranes  and  conjunctiva;,  and  a  darker  color  of  the  blood  in  the 
ear  veins.    Death  occurred  in  from  four  to  six  hours.    He  found  that 

1  Arch.  Int.  Med.,  1910,  v,  406.  2  Jour.  Exp.  Med.,  1913,  vol.  xvii,  No.  5. 

3  Ibid.,  1913,  vol.  xviii,  No.  1. 
12 


178  DISEASES  OF  THE  LUNGS 

the  oxygen  combining  power  of  the  blood  fell  progressively  up  to  the 
time  of  death,  due  to  the  conversion  of  hemoglobin  into  methemo- 
globin.  In  patients  with  lobar  pneumonia,  Peabody1  found  that  in 
most  cases  the  oxygen  content  of  the  blood  was  within  normal  limits, 
the  decrease  in  respiratory  surface  being  completely  compensated. 
But  in  the  terminal  stage  of  the  fatal  cases  in  which  death  did  not 
occur  with  great  suddenness,  there  was  often  a  progressive  diminution 
in  the  oxygen  content,  and  at  the  same  time  a  progressive  decrease 
in  the  oxygen  combining  capacity  of  the  blood.  These  changes,  usually 
seen  in  patients  in  whom  an  intense  bacteriemia  developed,  were 
probably  due  to  a  change  of  oxyhemoglobin  to  methemoglobin,  and 
may  be  regarded  as  a  probable  factor  in  the  immediate  cause  of  death 
in  many  cases  of  pneumonia.  Cole2  finds  that  the  transformation 
into  methemoglobin  takes  place  only  when  the  pneumococci  are  living. 

Carbon-dioxide  Content  of  the  Blood. — A  diminution  in  the  carbon 
dioxide  content  of  the  blood  in  fever  has  been  established  by  various 
observers,  and  is  generally  ascribed  to  a  lowered  alkalinity  of  the  blood. 
Loewy3  states  that  the  carbon-dioxide  content  of  venous  blood  nor- 
mally is  from  43  to  50  per  cent,  at  a  tension  of  40  to  50  mm.  of  mercury. 
Peabody4  finds  it  to  be  between  54  and  58  per  cent.  Peabody  made 
91  analyses  on  26  patients  with  pneumonia.  With  the  exception  of 
2  cases,  the  carbon  dioxide  was  found  to  be  regularly  diminished  during 
the  febrile  period,  and  in  most  cases  was  from  40  to  50  per  cent,  in  the 
acute  stage  of  the  disease,  but  not  infrequently  from  50  to  53  per  cent, 
or  only  slightly  below  normal.  The  lowest  observation  was  29.01 
per  cent.  The  carbon-dioxide  content  bears  little  definite  relation 
to  the  severity  of  the  disease,  except  that  it  tends  to  be  lowest  in 
severe  cases  and  in  the  terminal  stages  of  the  disease,  with  less  devia- 
tion from  the  normal  in  short  or  mild  cases.  The  diminution  bears 
no  immediate  relation  to  the  temperature,  as  it  may  persist  for  some 
days  after  defervescence.  The  diminution  in  carbon  dioxide  corre- 
sponds to  the  other  evidences  of  metabolic  changes  in  infection  and, 
like  them,  may  be  even  greater  after  than  during  the  febrile  period. 
The  changes  in  the  carbon-dioxide  content  of  the  blood  run  parallel 
to  the  output  of  ammonia  in  the  urine,  and  appear  to  bear  no  relation 
to  chlorine  excretion.  In  two  of  Peabody's  cases  the  carbon-dioxide 
content  of  the  blood  was  normal  or  above  normal,  and  this  was  asso- 
ciated with  a  very  low  oxygen  content  of  the  venous  blood. 

Inorganic  Substances. — The  chlorids  of  the  urine  are  greatly  dimin- 
ished, and  may  be  absent  during  the  course  of  the  disease  to  return 
to  normal  after  the  crisis.  Analyses  have  shown  that  too  little  is 
stored  in  the  consolidated  lung  to  account  for  the  suppression,  and 
that  retention  elsewhere  in  the  body  must  take  place.    It  is  generally 

1  Jour.  Exp.  Med.,  1913,  vol.  xviii,  No.  1. 

2  Jour.  Exp.  Med..  1914,  xx,  363. 

3  Loewy,  A.  in  von  Koranyi,  A.,  and  Richter,  P.  F.,  Physikalische  Chemie  und  Medizin, 
Leipzig,  1907,  i,  255. 

4  Jour.  Exp.  Med.,  1912,  vol.  xvi,  No.  5. 


LOBAR  PNEUMONIA  179 

believed  that  retention  occurs  throughout  the  fixed  tissues.  Hutch- 
inson1 and  Hosslin  and  Kashiwado2  regarded  the  permeability  of  the 
kidney  as  an  insignificant  factor.  Madigreceanu,3  as  a  result  of  the 
study  of  chlorin  metabolism  in  animals  with  experimental  pneumonia, 
general  pneumococcus  septicemia  and  pleural  exudates  induced  by 
means  of  turpentine,  concluded  that  the  formation  of  the  exudate 
is  only  one  factor  and  alone  incapable  of  producing  such  a  degree  of 
retention  as  occurs  in  pneumonia. 

The  investigations  of  Salkowski4  showed  that  sodium  as  well  as 
chlorin  was  retained.  Moraczewski5  demonstrated  a  retention  of 
calcium,  but  no  evidence  of  retention  of  magnesium.  Peabody6 
found  that  while  chlorin,  sodium  and  calcium  are  retained,  potassium 
and  magnesium  are  excreted  normally  or  in  excess.  Two  cases  showed  a 
definite  loss  to  the  body  of  magnesium  during  the  febrile  period.  He 
also  found  that  during  the  period  of  retention  the  chlorin  content  of  the 
blood  is  distinctly  lower  than  normally,  the  calcium  content  is  apparently 
slightly  lower,  and  the  magnesium  content  tends  also  to  be  a  little  lower. 

Pathology. — Since  Laennec's  time  pathologists  have  recognized 
three  stages  in  croupous  pneumonia,  i.  e.,  engorgement,  red  and  gray 
hepatization. 

The  stage  of  engorgement  is  rarely  observed  alone,  but  may  be 
seen  at  the  periphery  of  pulmonary  tissue  already  the  seat  of  a  more 
advanced  inflammation.  The  tissue  is  deep  red  in  color,  more  volu- 
minous than  normal,  and  abnormally  heavy.  On  section  a  serous, 
slightly  bloody  fluid  exudes.  It  is  doughy  to  feel,  still  crepitates,  and 
excised  portions  float  in  water.  On  microscopic  examination,  the 
capillaries,  smaller  arteries  and  veins  are  found  engorged  with  blood. 
The  alveolar  epithelium  is  swollen  and  the  alveoli  contain  a  variable 
and  usually  small  amount  of  serous  fluid,  red-blood  corpuscles,  and 
desquamated  epithelium.  Small  strands  of  fibrin  may  be  seen.  This 
stage  probably  lasts  but  a  few  hours  as  a  rule. 

In  the  stage  of  red  hepatization,  the  lung  tissue  is  solid,  reddish 
brown  in  color,  still  more  voluminous,  and  shows  indentations  from 
the  ribs.  It  is  friable,  firm  and  airless,  excised  portions  sinking  in 
water.  The  cut  surface  is  dry  and  granular.  A  small  amount  of  red- 
dish-brown, somewhat  viscid  fluid,  containing  small  granular  masses, 
may  be  scraped  from  the  cut  surface  with  the  knife.  The  fluid  is  more 
viscid  when  the  infection  is  due  to  streptococcus  mucosus  capsulatus. 
The  granular  appearance  is  due  to  the  expression  of  fibrinous  masses 
from  the  elastic  alveoli.  The  distinctness  with  which  they  can  be 
seen  varies  with  the  age  of  the  patient  and  the  consequent  size  of  the 
alveoli.     Damoschino7  states  that  in  children  the  granulations  have 

1  Jour.  Path,  and  Bact.,  1898,  v,  422.         2  Deut.  Arch.  f.  klin.  Med.,  1911,  cii,  520. 

3  The  Mechanism  of  Chlorin  Retention  in  Pneumonia,  Jour.  Exp.  Med.,  1911,  xiv,  289. 

4  Virchow's  Arch.  f.  path.  Anat.,  1871,  liii,  209. 

6  Ibid.,  1899,  civ,  11,  and  Zeit.  f.  klin.  Med.,  1900,  xxxix,  44. 

6  Jour.  Exp.  Med.,  1913,  vol.  xvii,  No.  1. 

7  Des  different  formes  de  la  pneumonie  aigue  chez  les  enfants,  Paris,  1867. 


ISO  DISEASES  OF  THE  LUNGS 

a  diameter  of  0.07  to  0.11  nam.,  in  adults  0.13  to  0.17,  and  in  the  aged 
0.21  to  0.27  nun.  When  the  pneumonia  affects  a  lung,  the  site  of 
emphysema,  the  granules  may  attain  an  unusually  large  size.  Fibrin- 
ous plugs  may  be  found  in  the  smaller  bronchi.  The  pleura  adjoining 
the  inflamed  lung  is  clouded  and  covered  with  a  fibrinous  layer.  On 
microscopic  examination  the  alveolar  walls  are  found  to  be  infiltrated 
and  their  lumen  filled  with  serum,  fibrin,  polynuclear  and  mononu- 
clear leukocytes,  and  desquamated  epithelium.  The  terminal  bronchi 
contain  a  similar  exudate.  The  fibrin  is  in  the  form  of  a  network, 
which  is  most  dense  in  the  neighborhood  of  the  alveolar  wall  and  forms 
a  wider  mesh  in  the  central  part  of  the  alveolar  space.  Isolated  fibers 
or  bundles  of  fibers  of  fibrin  may  be  seen  to  pass  through  the  alveolar 
wall  from  one  alveolus  to  another,  normal  openings  through  which 
such  a  communication  can  be  established,  having  been  demonstrated 
by  Hansemann1  in  the  lungs  of  animals.  The  reddish-brown  color 
of  the  tissue  is  due  to  the  presence  of  red-blood  corpuscles  and  hemo- 
globin in  the  exudate  and  to  the  congestion  of  the  bloodvessels.  The 
lymph  vessels  are  filled  with  serum,  leukocytes  and  fibrin,  which  may 
be  in  such  abundance  as  to  outline  their  course  in  the  interstitial  tissue. 

In  the  stage  of  gray  hepatization,  the  reddish-browm  color  of  the 
tissue  has  changed  to  grayish  or  grayish  white.  The  change  from  red 
to  gray  hepatization  is  gradual  and  not  everywhere  with  equal  rapidity, 
so  that  oftentimes  both  may  be  seen  together  in  the  same  lung,  giving 
it  a  spotted,  marble-like  appearance.  The  cut  surface  is  more  moist, 
still  granular  and  friable,  and  on  scraping  yields  a  more  turbid  fluid. 
The  granular  appearance,  though  still  present,  is  less  distinct.  Exami- 
nation with  the  microscope  explains  the  changed  appearance  of  the 
tissue.  There  is  less  blood  and  a  larger  number  of  white  cells,  while 
the  fibrin  is  much  diminished  or  has  disappeared.  The  compression 
of  the  bloodvessels  and  partial  obliteration  of  their  lumen  by  fibrin 
or  thrombi  are  in  part  responsible  for  the  color  of  the  tissue. 

With  the  advancement  of  the  process  the  more  cellular  becomes  the 
exudate.  In  the  stage  of  purulent  softening  or  resolution  the  pul- 
monary tissue  is  soft,  loses  its  granular  character,  and  on  pressure 
exudes  an  abundant  yellowish,  purulent  fluid.  The  process  differs 
from  ordinary  suppuration  in  the  rapid  disintegration  of  the  fibrin 
and  cellular  elements  and  their  disappearance.  On  microscopic 
examination  the  white  cells  show  fatty  degeneration  and  the  fibrin 
granular  degeneration.  The  final  disappearance  of  the  exudate  cannot 
be  ascribed  entirely  to  expectoration,  for  in  some  cases  both  cough 
and  expectoration  are  absent  from  beginning  to  end  of  the  disease. 
In  some  cases  resolution  may  proceed  to  completion  within  twelve 
to  twenty-four  hours,  to  judge  from  physical  examination. 

Autolysis. — The  exudate  must  therefore  disappear  largely  through 
absorption.     According  to  the  investigations  of  Fr.  Miiller2  and  O. 

1  Sitzungsber.  d.  Kgl.  Preuss.  Akad.  d.  Wissenschaften,  1895,  xliv,  199. 

2  Verhandl.  d.  Naturforschergesellsch.  in  Basel,  1901,  Bd.  xiii. 


LOBAR  PNEUMONIA  181 

Simon,1  the  exudate  probably  disappears  as  a  result  of  autolysis. 
Simon  observed  autodigestion  in  gray  hepatization  to  a  greater  degree 
than  in  red  hepatization,  and  this  was  later  confirmed  by  Silvestrius2 
and  Flexner.3  A  ferment-like  substance  is  probably  set  free  by  the 
leukocytes  and  liquefies  the  exudate.  This  autodigestion  may  be 
observed  in  vitro  if  pieces  of  pulmonary  tissue  in  the  stage  of  gray 
hepatization  are  preserved  in  the  incubator.  The  action  of  bacteria 
is  excluded  by  the  addition  of  toluol.  As  a  result  of  the  splitting  of 
the  proteid,  such  products  as  leucsin,  tyroin,  lysin  and  probably  histidin 
may  be  found.  Mayeda,4  after  autodigestion  of  the  lung  in  the  stage 
of  gray  hepatization,  found  splitting  of  the  nuclein  substances  with  the 
formation  of  xanthin  in  considerable  amount,  but  the  other  purin 
bases  (guanin,  adenin  and  hypoxanthin)  could  not  be  found.  The 
presence  of  free  uric  acid  in  the  autolyzed  pneumonic  lung  was  also 
established.  Nukada5  has  since  succeeded  in  isolating  uric  acid  from 
the  pneumonic  lung. 

Site  of  the  Disease. — In  practically  all  large  series  of  cases,  the  most 
frequent  site  of  the  disease  is  in  the  lower  lobes,  of  which  the  right  is 
the  more  frequently  affected.  In  Jurgensen's6  6666  cases  the  right 
lung  was  involved  alone  in  more  than  one-half  (53.7  per  cent.),  the  left 
lung  in  a  little  more  than  one-third  (38.23  per  cent.),  and  in  a  much 
smaller  number  (8.07  per  cent.)  both  lungs  were  invaded.  Among 
Frankel's7  830  cases,  he  noted  an  involvement  of  the  upper  lobes 
in  136  (16.4  per  cent.)  cases  and  central  pneumonia  in  only  14  (1.7 
per  cent.).  The  predominance  of  the  disease  on  the  right  side  and  in 
the  right  lower  lobe  has  been  ascribed  to  the  larger  size  and  straighter 
course  of  the  right  primary  bronchus,  from  which  the  branch  to  the 
right  lower  lobe  is  a  direct  continuation. 

The  affected  part  of  the  lung  may  present  different  stages  of  the 
disease  in  different  places  or  uniform  involvement  in  one  stage.  Accord- 
ing to  Tendeloo,8  when  the  former  condition  obtains,  the  central  parts 
are  in  the  most  advanced  stage,  as,  for  example,  in  resolution  or 
gray  hepatization;  and  from  the  centre  toward  the  periphery  gray- 
red,  red  hepatization,  inflammatory  engorgement,  and  in  the  adjacent 
tissue  often  stasis  or  acute  collateral  edema. 

Pneumococci  can  usually  be  demonstrated  in  cover-glass  prepara- 
tions from  the  exudate  in  early  cases  of  pneumonia.  Other  organ- 
isms are  frequently  present  also,  both  in  fresh  material  and  in 
cultures  from  the  lung.  Such  organisms  may  be  secondary  invaders 
or  indicate  postmortem  contamination  of  the  tissue.  In  sections  from 
croupous  pneumonia,  in  the  stage  of  red  or  gray  hepatization,  the 

1  Deut.  Arch.  f.  klin.  Med.,  1901,  Bd.  Ixx.  2  Bioch.  Zentralb.,  1903,  Bd.  i. 

3  Trans.  Assoc.  Amer.  Phys.,  1903,  vol.  xviii. 

4  Deut.  Arch.  f.  klin.  Med.,  1909-10,  xcviii,  587. 

5  Deut.  med.  Woch.,  1912,  No.  23,  p.  1090. 

6  Ziemssen's  Handb.  d.  spec.  Path.  u.  Ther.,  1874,  p.  51. 

7  Spec.  Path.  u.  Ther.  d.  Lungenkrankheiten,  1904,  p.  274. 

8  Studien  iiber  die  Ursachen  der  Lungenkrankheiten,  Wiesbaden,  1902,  p.  225. 


1S2  DISEASES  OF  THE  LUNGS 

pneumococci  may  often  be  found  in  enormous  numbers  both  within 
and  without  the  cells.  With  the  advancement  of  the  process  they  are 
more  difficult  of  demonstration. 

The  bronchi  are  usually  injected  and  their  finer  ramifications  may 
contain  fibrinous  casts.  Both  visceral  and  parietal  pleurae  are  almost 
without  exception  inflamed  over  the  region  of  pulmonary  involvement. 
At  autopsy  a  small  amount  of  cloudy  fluid  is  usually  present  in  the 
pleural  sac.  On  microscopic  examination  this  is  found  to  contain 
a  predominance  of  polynuclear  leukocytes  with  a  few  endothelial  and 
small  mononuclear  cells.  The  mediastinal  lymph  glands,  especially 
those  about  the  larger  bronchi,  are  frequently  enlarged.  Of  other 
organs  the  spleen  is  often  large  and  soft.  The  heart  is  frequently 
dilated  and  may  contain  thrombi.  Both  dilatation  and  thrombus 
formation  affect  for  the  most  part  the  right  auricle  and  ven- 
tricle. 

Accidents  of  Resolution. — Organizing  Pneumonia. — A  termination 
of  the  pneumonia  in  organization  rather  than  resolution  occurs  in  a 
small  proportion  of  cases.  Among  210  cases  at  the  Massachusetts 
General  Hospital  with  genuine  croupous  pneumonia  at  autopsy,  or 
with  a  history  which  may  be  interpreted  as  lobar  pneumonia,  were  16 
(7.6  per  cent.)  of  organizing  or  indurative  pneumonia.  Replacement 
of  the  inflamed  tissue  by  connective  tissue  finally  transforms  it  into  a 
dense,  firm,  airless,  and  contracted  mass  of  scar  tissue.  A  termination 
in  organization  and  fibrosis  is  responsible  for  the  condition  spoken 
of  clinically  as  delayed  resolution.  In  its  clinical  aspects  organizing 
pneumonia  is  more  fully  discussed  under  delayed  resolution.  The 
subject  is  also  considered  in  the  chapter  on  Subacute  and  Chronic 
Indurative  Pneumonia,  of  which  organizing  croupous  pneumonia  is 
an  important  cause. 

Abscess  and  Gangrene. — In  51  cases  of  croupous  pneumonia  coming 
to  autopsy  at  the  Massachusetts  General  Hospital,  pulmonary  losses 
of  substance  either  micro-  or  macroscopically,  were  found  in  14  (27 
per  cent.).  Croupous  pneumonia  is  one  of  the  most  important  causes 
of  abscess  and  gangrene  for  which  the  compression  of  the  bloodvessels 
by  the  exudate  and  their  partial  or  complete  obliteration  by  thrombi 
may  be  responsible.  For  further  discussion,  the  section  on  Abscess 
and  Gangrene  may  be  consulted. 

Incubation  Period. — This  is  probably  short.  To  judge  from  trau- 
matic cases  it  may  be  placed  at  from  one  to  two  days.  Certain  epidemic 
cases  suggest  that  it  may  last  as  long  as  eight  days. 

Prodromata. — The  most  constant  symptoms  preceding  the  onset 
are  those  of  a  mild  acute  respiratory  infection.  A  history  of  a  "cold" 
from  a  few  days  to  several  weeks  before  the  onset  and  usually  accom- 
panied or  followed  by  cough  was  obtained  in  31  of  200  cases  of  pneu- 
monia. The  respiratory  infection  does  not  appear  to  differ  from  an 
ordinary  "  cold"  until  the  patient  is  suddenly  stricken  with  pneumonia. 
In  other  and  less  common  instances  malaise,  general  pains,  headache, 


LOBAR  PNEUMONIA  183 

chilliness  and  fever  may  be  present  for  a  clay  or  two  before  the  more; 
striking  features  of  the  onset  develop. 

Symptoms. — These  are  both  local  and  general.  The  local  features 
are  referable  to  the  changes  in  the  lung  and  neighboring  tissues  in 
consequence  of  the  infection  with  pneumococci.  The  general  symptoms 
are  such  as  are  observed  in  other  infections.  In  the  case  of  the  pneu- 
mococcus  infections  they  are  probably  due  to  toxemia  in  consequence 
of  destruction  of  the  organisms  and  the  setting  free  of  intracellular 
poisons. 

General  Clinical  Description. — The  onset  is  usually  abrupt  and  with 
pain  in  the  side,  cough  and  chill  or  chilliness  in  a  very  large  proportion 
of  the  cases.  The  pain,  cough,  and  chill  are  usually  coincident.  The 
pain  is  commonly  a  very  distressing  symptom  and  is  aggravated  by 
exertion,  deep  breath  or  cough,  and  increases  the  dyspnea  by  limiting 
respiratory  motion.  The  cough  is  at  first  dry  and  painful.  The 
sputum  usually  becomes  rusty  within  twenty-four  hours.  The  chill 
lasts  from  a  half-hour  to  several  hours,  and  is  accompanied  or  followed 
by  a  rapid  rise  of  temperature,  which  may  reach  102°  to  104°  within 
a  few  hours.  A  rise  in  the  frequency  of  the  pulse  and  respiration 
accompanies  the  symptoms  of  invasion.  The  normal  relation  of  respi- 
ration to  pulse  may  be  much  disturbed,  the  former  being  increased  out 
of  proportion  to  the  latter.  The  patient  is  frequently  found  lying 
on  the  affected  side,  the  alee  nasi  dilating  with  inspiration,  an  audible 
grunt  with  expiration.  The  face  is  likely  to  be  flushed  and  the  lips 
cyanotic.  Herpetic  lesions  may  be  present,  but  are  seldom  observed 
before  the  second  or  third  day.  If  the  patient  is  seen  within  twenty- 
four  hours  of  the  onset,  the  physical  signs  are  usually  limited  to  slight 
dulness  and  fine  consonating  rales  with  long  breath  or  cough.  Harsh 
inspiration,  bronchovesicular  breathing  and  slight  changes  in  the  voice, 
whisper  and  tactile  fremitus  may  be  demonstrable,  but  are  often 
lacking.  Diminished  breathing  may  be  the  only  sign.  In  some  cases 
at  this  early  period  the  lungs  are  negative.  Usually  by  the  second  or 
third  day  the  pulmonary  findings  are  outspoken.  Inspection  shows 
restricted  motion  of  the  affected  side,  over  which  there  is  dulness, 
bronchial  breathing,  increased  voice,  whisper  and  tactile  fremitus.  In 
the  absence  of  diffuse  bronchitis,  fine  consonating  rales  can  usually  be 
heard  over  the  involved  region  during  the  early  period  of  the  disease, 
but  may  disappear  while  it  is  at  its  height.  In  typical  cases  the  extent 
of  the  involvement  gradually  increases  until  involvement  of  the  greater 
part  or  the  whole  of  one  lobe  may  be  determined.  In  atypical  cases 
the  evidence  on  physical  examination  may  be  uncertain  for  a  time 
or  remain  so  throughout  the  disease.  In  from  five  to  ten  days  the 
temperature  usually  falls  by  crisis  or  lysis,  and  with  defervescence 
signs  of  resolution  may  be  heard  in  the  affected  lung.  The  fine  con- 
sonating rales,  redux  crepitus,  of  the  period  of  invasion  return  and  the 
percussion  note  becomes  more  resonant.  The  rusty  color  of  the  sputum 
gives  place  to  a  more  purulent  and  less  tenacious  expectoration. 


184  DISEASES  OF  THE  LUNGS 

In  any  large  series  of  eases  the  course  of  the  disease  is  very  variable. 
All  grades  of  severity  may  be  observed.  In  the  mildest  eases  the  patient 
may  be  quite  comfortable  throughout.  The  sputum  may  be  scanty 
or  absent  and  the  cough  not  discomforting.  There  may  be  no  pain, 
and  the  pulse  and  temperature  little  elevated.  Hardy  subjects  may 
continue  their  occupation  as  in  the  case  of  a  man  of  thirty-one  with  a 
history  of  pain,  cough  with  blood-streaked  sputum  and  chill  six  days 
before  entrance,  who  worked  as  a  cigar-maker  until  he  fainted  in  the 
shop  the  day  before  admission.  The  temperature  may  begin  to  fall 
in  rare  instances  by  the  third,  but  more  often  in  mild  cases  by  the  fifth 
day.  Even  in  mild  eases  predictions  are  unsafe  and  there  may  be  a 
rapid  transition  from  a  condition  of  apparent  safety  to  one  of  great 
gravity.  Such  changes  are  usually  gradual,  however,  and  indicated 
by  greater  cyanosis,  more  rapid  pulse  and  respiration,  extension  of  the 
pulmonary  lesions,  restlessness,  insomnia,  and  delirium.  The  severity 
of  the  general  symptoms  is  a  better  indication  of  progress  than  the 
extent  of  the  pulmonary  involvement.  Bilateral  or  multiple  lobar 
involvement  is  less  favorable. 

Special  Symptoms. — A  chill  usually  marks  the  onset  and  from  it  the 
duration  of  the  disease  is  reckoned.  It  was  present  in  only  about  a 
half  of  my  series.  Louis  noted  chills  in  61  (77  per  cent.)  of  79  cases 
and  Grisolle  145  times  (79  per  cent.)  in  182  cases.  Chilliness  may 
replace  the  chill.  Chill  is  likely  to  be  absent  at  the  extremes  of  age,  in 
alcoholic  subjects,  and  when  pneumonia  complicates  acute  or  chronic 
disease. 

Fever. — The  fever  usually  begins  to  rise  with  the  initial  chill,  and 
may  reach  its  maximum  within  twelve  to  twenty-four  hours.  In  rare 
instances,  the  fastigium  is  reached  only  after  several  days,  during  which 
the  evening  record  is  slightly  higher  than  that  of  the  previous  day. 
Having  reached  its  height,  the  temperature  is  commonly  remittent 
with  a  morning  remission  of  from  one  to  two  or  more  degrees.  More 
constant  fever  with  variations  of  only  a  degree  or  less  between  the 
morning  and  evening  record  is  occasionally  seen.  On  the  other  hand, 
well-marked  daily  remissions  or  even  intermissions  may  be  observed. 
In  the  aged,  and  in  debilitated  subjects,  with  chronic  disease,  an  other- 
wise typical  pneumonia  may  be  afebrile.  Immediately  preceding  the 
termination  of  the  disease  the  temperature  occasionally  rises  above 
its  previous  level.  From  102°  to  104°  is  an  average  pyrexia.  Fever 
of  105°  to  106°  is  uncommon  and  107°  was  reached  only  once  in  my 
series.  Of  1987  cases  collected  by  Musser  and  Norris,  the  fever  ter- 
minated in  from  five  to  ten  days  in  1405  (70  per  cent.).  A  pneumonia  of 
two  and  three  days'  duration  is  occasionally  seen.  On  the  other  hand 
the  disease  may  run  a  protracted  course  of  two  to  three  weeks  or  more. 

Defervescence  is  more  often  by  crisis  in  which  the  temperature 
returns  to  normal  within  twelve  to  twenty-four  hours.  If  the  fall  is 
prolonged  for  twenty-four  to  thirty-six  hours,  it  is  spoken  of  as  a  pro- 
tracted crisis.    Toward  the  end  of  the  disease  there  may  be  a  rapid 


LOBAR  PNEUMONIA  185 

fall  of  temperature  followed  by  a  rapid  rise.  This  fall  is  spoken  of  as 
a  pseudocrisis.  Defervescence  usually  occurs  in  the  late  evening 
hours  and  the  signs  of  beginning  resolution  commonly  just  precede, 
accompany  or  follow  it.  Crisis  is  more  common  in  children,  in  vigorous 
adults  and  in  cases  running  a  brief  course.  Complications  are  less 
frequently  observed  in  cases  terminating  by  crisis.  Defervescence 
which  lasts  longer  than  thirty-six  hours  is  spoken  of  as  lysis.  It  is 
more  common  in  the  aged,  those  subject  to  acute  or  chronic  disease, 
debilitated  patients  and  in  the  presence  of  complications.  Complica- 
tions are  nearly  four  times  more  frequent  in  cases  terminating  by  lysis 
than  by  crisis. 

The  fall  of  the  temperature  by  crisis  and  less  commonly  by  lysis 
may  be  followed  by  such  symptoms  of  exhaustion  as  sweating  and 
rapidity  and  weakness  of  the  pulse.  A  subnormal  temperature  for 
several  days  after  defervescence  is  common.  In  some  cases  there  is 
a  slight  evening  rise  of  temperature  for  several  days. 

Cyanosis. — This  is  almost  invariably  present  and  increases  as  the 
disease  progresses.  It  is  probably  in  part  due  to  diminished  respira- 
tory area,  restricted  respiratory  motion  from  pain  and  mechanical 
interference  with  the  pulmonary  circulation.  The  investigations  of 
Peabody  (quoted  under  Metabolism)  suggest  that  a  low  oxygen 
capacity  of  the  blood  and  the  formation  of  methemoglobin  as  a  result 
of  the  pneumococcus  infection  may  also  be  in  part  responsible. 

Respiratory  Symptoms. — Pain  is  the  most  striking  and  constant 
of  the  triad  of  initial  symptoms — pain,  cough  and  chill,  and  is  due  to 
invasion  of  the  pleura.  It  was  present  in  272  (88  per  cent.)  of  Grisolle's 
309  patients  and  in  89  out  of  100  cases  in  the  Massachusetts  General 
Hospital  series.  The  pain  is  often  described  as  a  "stitch  in  the  side" 
and  is  usually  coincident  with  the  chill  and  cough.  It  is  commonly 
severe  enough  to  make  the  patient  cry  out,  double  him  up  and  awake 
him  from  sleep.  It  is  of  abrupt  onset,  lancinating  in  character  and 
usually  felt  in  the  lower  lateral  thoracic  region  on  the  affected  side, 
but  may  be  referred  to  the  shoulder,  abdomen  or  hip.  In  rare  instances 
it  is  felt  on  the  unaffected  side.  It  is  less  intense  and  may  be  absent 
in  children,  in  apical  or  central  pneumonia  and  in  delirious  patients. 
When  severe,  it  contributes  to  the  dyspnea  and  is  usually  aggravated 
by  long  breath,  cough,  sneezing,  and  talking.  Amelioration  follows 
immobilizing  the  chest.  Cutaneous  hyperesthesia  over  the  painful 
region  may  also  be  noted.  With  the  progress  of  the  disease  the  pain 
diminishes  or  disappears,  and  is  not  a  prominent  feature  toward  the 
latter  part  of  the  illness. 

Abdominal  pain  as  an  initial  symptom  may  lead  to  the  confusion  of 
pneumonia  with  an  acute  abdominal  affection  such  as  gall-stones  or 
appendicitis.  It  was  noted  in  12  out  of  200  cases  in  this  series.  It  is 
usually  referred  to  the  upper,  but  may  be  felt  in  the  lower  quadrants  of 
the  abdomen.  Spasm  and  tenderness  may  accompany  the  pain.  It 
is  probably  due  to  irritation  of  the  terminal  branches  of  the  lower  six 


186  DISEASES  OF  THE  LUNGS 

intercostal  nerves  which  supply  the  abdominal  wall  with  sensation. 
The  eleventh  nerve  supplies  the  abdominal  wall  over  the  appendix 
region. 

Respiration. — The  character  of  the  respiration  is  one  of  the  striking 
features  of  the  disease.  In  typical  cases  the  respiratory  movements 
are  restricted  and  short,  with  inspiratory  dilatation  of  the  alas  nasi 
and  "expiratory  grunt."  An  increase  in  the  rate  of  respiration  to  30 
or  more  per  minute  was  observed  in  all  but  9  of  200  cases,  from  30  to 
40  in  78  (39  per  cent.),  from  40  to  50  in  60  (30  per  cent.),  and  from 
50  to  60  in  25  (12.5  per  cent.).  An  elevation  to  60  or  more  is  occasion- 
ally observed  in  adults.  In  children,  a  rate  of  from  40  to  50  is  common 
and  may  rise  to  100  or  more.  Increased  respiration  in  pneumonia 
is  due  to  restriction  of  respiratory  excursion  from  pain,  to  exclusion 
of  the  involved  part  of  the  lung  from  participation  in  respiration, 
to  fever,  toxemia,  and  cyanosis.  The  rate  of  respiration  is  of  only 
limited  value  in  prognosis,  but  the  mortality  in  adults  is  above  the 
average  among  those  with  a  rate  of  50  or  over.  Varying  grades  of 
dyspnea  usually  accompany  the  increase  in  the  rate  of  respiration. 

Cough  is  almost  invariably  present  at  some  time  during  the  course 
of  the  disease.  It  is  usually  an  initial  symptom  occurring  simulta- 
neously with  the  chill  and  pain  in  the  side.  In  some  cases  it  is  delayed 
for  a  few  hours  or  a  day  or  more.  It  is  a  less  prominent  feature  and 
may  be  absent  when  the  upper  lobes  are  involved,  in  the  aged,  in  delir- 
ious patients,  and  in  those  already  subject  to  acute  or  chronic  disease. 
Von  Jiirgensen  justly  remarks  that  "Cough  is  rarely  of  use,  always 
troublesome  and  sometimes  dangerous."  It  may  exhaust  the  patient's 
strength,  disturb  his  sleep  aggravate  the  pleural  pain,  and  overtax 
the  right  side  of  the  heart  by  increasing  intrapulmonary  pressure. 
It  is  at  first  dry,  but  later  productive,  and  then  more  often  necessary 
for  the  elimination  of  secretion.  Sudden  cessation  of  cough  may 
indicate  approaching  exhaustion,  stupor  or  coma. 

Sputum. — In  about  one-half  to  three-quarters  of  the  cases  of 
croupous  pneumonia  (in  62  per  cent,  of  my  series),  the  sputum  is 
quite  typical  of  the  disease.  It  is  rusty,  tenacious,  glairy,  and  trans- 
parent. The  rusty  sputum  appears  usually  in  the  course  of  the  first 
or  second  day,  but  may  not  appear  until  the  latter  days  of  the  illness. 
The  brick-dust  appearance  is  due  to  admixture  with  the  blood  cor- 
puscles and  hemoglobin.  In  other  cases,  the  sputum  fails  to  show 
a  rusty,  tenacious  character,  and  is  white  and  mucoid,  yellowish  or 
greenish  and  mucopurulent.  It  may  consist  of  almost  pure  pus. 
Sputum  of  this  character  is  probably  due  to  the  accompanying 
bronchitis.  During  the  stage  of  resolution  the  rusty  color  begins  to 
disappear,  and  for  a  short  period  during  convalescence  the  patient 
continues  to  expectorate  diminishing  amounts  of  mucopurulent  or 
purulent  sputum.  The  amount  of  sputum  usually  averages  about  one 
to  two  ounces  in  the  twenty-four  hours,  the  exudate  being  for  the 
most  part  absorbed  rather  than  expectorated.    Expectoration  may  be 


LOBAR  PNEUMONIA  187 

absent  throughout  the  course  of  the  disease.  This  is  almost  invariably 
the  case  in  children  who  swallow  the  sputum,  and  is  common  in  the 
aged,  in  much  debilitated,  stuporous  or  delirious  patients. 

Hemorrhagic  sputum  may  be  seen  in  pneumonia  complicating  car- 
diac disease  with  broken  compensation,  and  in  pneumonia  following 
trauma.  When  it  occurs  in  other  cases,  pulmonary  tuberculosis 
should  be  suspected.  Strieker1  noted  hemoptysis  in  only  7  among 
16,711  cases  of  acute  pneumonia.  The  bloody  sputum  of  pulmonary 
infarction  may  closely  resemble  or  be  identical  with  that  in  lobar 
pneumonia,  but  is  usually  more  hemorrhagic,  darker  red,  and  less 
transparent.  The  sputum  from  cases  in  which  the  pneumonia  is  due 
to  infection  with  Friedlander's  bacillus  has  a  more  mucoid  and  stringy 
appearance. 

Biliary  coloring  matter  appears  to  be  a  constant  finding  in  pneu- 
monic sputum,  as  has  been  shown  by  Obermayer  and  Popper2  and 
Pollak3.  Herxfeld  and  Steiger4  found  that  the  different  tests  for 
biliary  coloring  matter  in  the  sputum  during  the  febrile  stage  were 
positive  even  in  cases  in  wrhich  no  subicteric  color  was  present  in  the 
skin  and  mucous  membranes.  They  also  found  in  typical  pneumonic 
sputum  in  many  cases  a  substance  which  gave  the  reactions  of  urobilin. 

On  careful  inspection  of  the  sputum  delicately  branched  white  to 
reddish  fibrinous  casts  can  at  times  be  found.  They  are  best  demon- 
strated by  teasing  the  specimen  apart  under  water.  Curschmann 
spirals  are  at  times  also  seen. 

Examination  of  the  Sputum  for  Pneumococci. — Care  should  be  used 
in  the  selection  of  masses  for  examination  to  take  the  more  suspicious 
particles.  A  small  mass  of  rusty,  tenacious  material  may  be  picked 
up  with  the  platinum  loop  or  small  forceps.  The  best  results  are 
obtained  if  the  mass  is  washed  of  adherent  mucus  in  sterile  salt  solu- 
tion, water  or  bouillon  before  examination.  Thin  smears  should  be 
made  on  cover-glasses  and  the  material  fixed  in  the  flame  in  the  ordi- 
nary way.  Loffler's  alkaline  methylene  blue  heated  in  the  Bunsen 
flame  for  a  few  seconds  stains  the  organisms  satisfactorily,  but  fails 
to  bring  out  the  capsule.  Carbol-fuchsin  (5  to  10  per  cent.)  may  be 
used  and  will  at  times  demonstrate  the  capsule.  By  these  methods 
the  morphology  of  the  organism  can  be  recognized  and  the  presence 
of  capsules  suspected  by  a  wide  unstained  zone  about  it.  The  use  of 
Gram's  stain  followed  by  a  saturated  aqueous  solution  of  eosin,  as 
in  Smith's5  method  is  most  satisfactory.  By  this  method  capsules, 
if  present,  are  usually  demonstrated.  All  specimens  should  also  be 
stained  for  the  tubercle  bacillus  as  part  of  the  routine  examination. 

Cultivation  of  Pneumococci. — Pneumococci  may  be  cultivated  from 
the  sputum  by  the  following  method :   Careful  washing  of  the  suspected 

1  Quoted  from  Sticker.     Nothnagel's  Spec.  Path.  u.  Ther.,  xiv,  Bd.  ii,  1  Abt. 

2  Wien.  klin.  Woch.,  1908,  No.  28.  3  Ibid.,  190S,  No.  27. 
4  Medizinische  Klinik,  1910,  No.  36,  p.  1415. 

6  Boston  Med.  and  Surg.  Jour.,  December  18,  1902. 


Ins  DISEASES  OF  THE  LUNGS 

mass  by  passage  through  several  tubes  of  sterile  solution  is  most  impor- 
tant in  obtaining  satisfactory  results.  The  sputum  mass  thus  freed 
of  adherent  mucus  may  then  be  smeared  on  the  surface  of  Loffler's 
slanted  blood-serum.  From  this  tube  at  the  time  of  inoculation,  other 
Tubes  should  be  inoculated  in  sequence  to  secure  complete  isolation 
of  colonies  after  incubation.  It  is  seldom  necessary  to  make  more  than 
three  or  four  such  dilutions.  The  rabbit  and  mouse  are  most  suscep- 
tible and  the  latter  most  often  used  for  testing  the  virulence  of  the 
organism.  Considerable  variation  in  infective  power  is  noted.  Inocu- 
lation with  fresh  sputum  may  be  made  subcutaneously  or  within  the 
peritoneum.  With  virulent  organisms  and  a  susceptible  animal, 
the  pneumococcus  can  be  recovered  from  the  heart's  blood  and  the 
spleen. 

Pneumococci  are  usually  present  in  large  numbers  in  the  sputum 
during  the  febrile  period,  but  rapidly  diminish  after  the  crisis  is  passed. 
For  the  identification  of  the  various  types,  a  study  of  their  morphology, 
cultural  peculiarities,  protection  experiments  in  animals  with  immune 
serum  and  agglutinative  reactions  may  be  necessary.  For  rapid  isola- 
tion of  the  organism  from  the  sputum  for  agglutinative  tests,  Dochez's 
method1  is  as  follows:  A  likely  mass  of  sputum  is  washed  several 
times  in  sterile  salt  solution,  rubbed  up  in  a  mortar  with  one-half 
a  cubic  centimeter  of  bouillon  and  injected  into  the  peritoneal  cavity 
of  a  mouse.  The  animal  is  killed  after  about  eight  hours  and  the  peri- 
toneal exudate  washed  out  with  5  to  6  c.c.  of  salt  solution  or  bouillon. 
This  suspension  of  bacteria  and  leukocytes  is  then  centrifuged  at  a 
rate  sufficient  to  throw  down  the  leukocytes.  The  supernatant  fluid 
is  withdrawn  and  centrifuged  rapidly  to  collect  the  bacteria.  A  dense 
emulsion  of  bacteria  thus  obtained  may  be  used  for  the  agglutinative 
tests. 

The  mere  presence  of  pneumococci  in  the  sputum  is  of  little  moment 
in  the  diagnosis  of  lobar  pneumonia,  since  these  organisms  are  not 
infrequently  the  cause  of  bronchitis  without  demonstrable  pulmonary 
lesions.  The  demonstration  of  pneumococci  in  a  rusty,  tenacious 
sputum  is  of  greater  importance,  but  cannot  be  regarded  as  con- 
clusive evidence  in  establishing  the  diagnosis.  Secondary  infection  of 
an  area  of  pulmonary  infarction  may  result  in  rusty  sputum  contain- 
ing pneumococci.  No  constant  relation  obtains  between  the  number 
of  pneumococci  in  the  sputum  and  the  severity  of  the  attack. 

Circulatory  System. — The  pulse  is  usually  strong  and  full  in  the  early 
stages  of  pneumonia  and  throughout  the  course  in  mild  cases.  In 
cases  of  moderate  severity,  the  rate  does  not  usually  rise  above  100 
to  110.  From  a  third  to  a  half  of  adult  patients  with  a  rate  of  120 
or  over  succumb  to  the  disease.  About  three-quarters  of  those  with 
a  rate  of  140  or  over  terminate  fatally.  In  one  of  my  cases  in  which 
pneumonia   complicated   chronic   mitral   endocarditis   and    auricular 

1  Personal  communication. 


LOBAR  PNEUMONIA  L89 

fibrillation,  the  cardiac  rate  was  counted  at  200  over  the  apex  and  yet 
recovery  followed.  The  pulse  is  more  rapid  in  women  and  in  those 
of  small  stature.  In  children  a  rate  of  120  to  150  or  more  is  common. 
Of  17  patients  with  an  irregular  pulse  13  died.  The  normal  relation 
of  the  respiration  to  the  pulse  of  about  1  to  4  is  usually  disturbed  in 
pneumonia  and  the  ratio  may  be  reduced  to  1  to  3,  1  to  2  or  even  1  to  1. 
Bradycardia  may  be  observed  in  the  first  few  days  after  the  crisis. 
Sphygmographic  tracings  show  that  the  dicrotic  notch  is  more  marked 
in  pneumonia  than  during  health,  but  it  is  unusual  to  be  able  to  dem- 
onstrate this  with  the  finger. 

Blood-pressure.- — Judging  from  152  cases  in  which  the  pressure  was 
measured  at  the  Massachusetts  General  Hospital,  there  is  no  note- 
worthy deviation  from  the  normal  in  pneumonia,  the  recorded  pressures 
being  what  might  be  expected  for  persons  in  health  and  usually  ranging 
from  110  to  130  mm.  of  mercury.  Crisis  appears  to  be  unaccompanied 
by  any  constant  change  in  the  pressure. 

The  Heart. — A  careful  note  of  the  condition  of  the  heart  should  be 
made  at  the  time  of  the  first  visit  in  patients  with  pneumonia.  The 
percussion  outline  of  the  deep  cardiac  dulness  and  the  point  farthest 
down  and  out  toward  the  left  at  which  the  cardiac  impulse  can  be 
palpated  should  be  noted  for  comparison  with  subsequent  findings 
when  the  question  of  displacement  from  pleural  effusion  or  variations 
in  consequence  of  pericardial  effusion  may  be  of  importance.  Careful 
percussion  usually  fails  to  show  any  noteworthy  change  in  the  cardiac 
outline  during  the  course,  even  of  severe  cases  with  cardiac  insufficiency. 
In  some  instances,  however,  an  increase  of  the  cardiac  dulness  beyond 
the  normal  limits  to  the  right  may  be  demonstrated.  This  may  be 
due  to  dilatation  of  the  right  side  of  the  heart  from  obstruction  of  the 
pulmonary  circulation.  Consolidation  of  a  considerable  volume  of  the 
lung  lying  next  the  heart  may  displace  it  slightly  away  from  the 
affected  region.  Solidification  on  one  side  in  a  region  remote  from  the 
heart  may  lead  to  slight  displacement  toward  the  affected  region  in 
consequence  of  compensatory  emphysema  of  the  other  and  uninvolved 
lung.  In  one  patient  (No.  190591),  in  whom  a  pneumonia  at  the  right 
base  developed  under  observation  in  the  hospital,  the  heart  was  dis- 
located 3  cm.  to  the  right  and  returned  to  its  previous  normal  position 
with  the  subsidence  of  the  pneumonia.  Pleural  effusion  displaces  the 
heart  away  from  the  affected  side.  When  the  right  middle  lobe  is 
consolidated,  it  may  be  difficult  or  impossible  to  outline  the  right 
border  of  the  heart. 

Systolic  soft  blowing  murmurs  over  the  precordia,  of  maximum  inten- 
sity at  the  apex  or  in  the  left  second  interchondral  space,  not  uncom- 
monly appear  during  the  course  of  pneumonia.  An  apical  systolic 
murmur  may  also  be  heard  in  the  axilla  and  even  in  the  back.  Such 
murmurs  may  be  unaccompanied  by  symptoms  or  signs  of  cardiac 
weakness,  disappear  during  convalescence,  and  are  to  be  regarded  as 
of  functional  origin.    They  are  probably  due  to  relaxation  of  the  myo- 


190  DISEASES  OF  THE  LUNGS 

cardium.  Organic  murmurs  may  be  due  to  a  complicating  acute  or 
preexistent  chronic  endocarditis. 

The  behavior  of  the  heart  may  be  of  great  importance  in  estimating 
the  chances  for  recovery  and  the  indications  for  treatment.  The 
second  pulmonic  sound  is  usually  accentuated  in  consequence  of  the 
increased  resistance  in  the  pulmonary  circuit,  and  daily  observation 
may  show  a  lessening  of  its  intensity  in  cases  in  which  the  heart  is 
failing.  Transmission  of  the  second  sound  through  neighboring  and 
consolidated  lung  may  intensify  it  and  thus  interfere  with  the  inter- 
pretation. A  shortening  of  the  first  cardiac  sound  and  approach  to 
the  second  in  quality  (embryocardia),  increased  rapidity  and  weakness 
of  the  pulse,  cyanosis,  aggravated  dyspnea,  with  or  without  nervous 
symptoms  may  come  on  gradually  or  suddenly.  Heart  weakness  is 
unusual  before  the  third  day.  It  is  not  uncommon  at  the  time  of  the 
expected  crisis,  and  in  rare  instances  may  occur  after  the  crisis  is 
successfully  passed.  Sudden  death  from  pulmonary  embolism  may 
occur  when  the  patient  sits  up  for  the  first  time. 

Skin. — Labial  herpes  occurs  more  frequently  in  pneumonia  than 
in  any  other  disease  and  may  thus  be  of  considerable  diagnostic  value. 
One  or  many  vesicles  may  be  present.  Herpes  may  also  appear  at  the 
angles  of  the  mouth,  about  or  just  within  the  nose,  on  the  chin,  genitals, 
about  the  anus  and  rarely  in  other  parts  of  the  body.  Various  observers 
have  noted  herpes  in  from  7  to  50  per  cent,  of  the  cases.  Of  200  cases 
at  the  Massachusetts  General  Hospital,  it  was  recorded  in  only  5  per 
cent.  The  eruption  usually  appears  about  the  third  day  of  the  disease, 
but  may  be  observed  at  any  time.  Howard1  found  congestion,  hemor- 
rhage, cellular  infiltration  and  degeneration  of  the  cells  in  the  Gasserian 
ganglion  in  cases  in  which  herpes  was  present  in  the  distribution  of 
the  fifth  nerve.  Herpes  has  been  regarded  as  a  sign  of  favorable 
import  in  pneumonia.  Of  395  cases  with  herpes  collected  by  Musser 
and  Norris,2  43  (10.8  per  cent.)  died,  of  239  without  herpes  70  (29.2 
per  cent.)  died.  Sweating  may  occur  during  the  course  of  the  dis- 
ease, but  is  uncommon.  It  is  more  often  seen  at  the  time  of  the  crisis. 
Sudamina  are  occasionally  observed.  Redness  of  one  cheek,  usually 
on  the  same  side  as  the  pneumonia,  may  occur.  Diffuse  erythema,  a 
roseola-like  eruption,  purpura  and  furunculosis  have  been  described. 

Urine. — This  usually  presents  the  characters  common  to  other  acute 
infections  with  fever,  and  is  diminished  in  quantity,  of  a  high  color, 
increased  acidity  and  high  specific  gravity.  The  quantity  is  often 
diminished  to  less  than  one-half  the  normal  during  the  disease  and 
commonly  arises  to  or  above  the  normal  during  crisis  or  lysis.  No 
constant  relation  appears  to  obtain  between  the  amount  of  urine  and 
the  favorable  or  unfavorable  outcome  of  the  disease.  The  high  color 
is  due  to  greater  concentration  and  increase  of  urobilin.  The  urea 
and  uric  acid  are  usually  relatively  and  absolutely  increased.    Nitrogen 

1  Amer.  Jour.  Med.  Sci.,  February,  1903. 

2  Osier.     Mod.  Med.,  vol.  ii,  p.  577. 


LOBAR  PNEUMONIA  191 

is  increased  during  resolution,  as  has  been  shown  by  Fr.  Miiller.1  If 
resolution  is  delayed,  an  excess  of  nitrogen  may  be  maintained  in  the 
urine  according  to  H.  W.  Cook's2  observations.  Pick3  observed  that 
the  acidity  of  the  urine  may  be  diminished  to  such  a  degree  as  to  become 
strongly  alkaline  in  the  first  few  days  after  the  crisis.  This  was  the 
case  in  31  of  38  cases  and  may  be  ascribed  to  increased  absorption 
of  fixed  alkali  from  the  resolving  exudate. 

The  chlorids  are  greatly  diminished  and  may  be  absent  during  the 
course  of  the  disease  to  return  to  normal  after  the  crisis,  as  mentioned 
under  Metabolism  in  Pneumonia.  Suppression  of  chlorids  has  no 
prognostic  significance.  It  is  more  common  in  pneumonia  than  in 
other  conditions  and  may  thus  have  a  limited  diagnostic  value. 

Of  abnormal  substances  in  the  urine,  acetone  may  be  found  as  in 
other  febrile  diseases.  The  diazo-reaction  may  be  present,  but  is  less 
common  than  in  typhoid  fever.  Traces  of  albumin  are  common  and 
were  found  in  71  of  100  cases  at  the  Massachusetts  General  Hospital. 
Even  a  considerable  quantity  of  albumin  with  tube  casts  and  blood 
may  be  due  merely  to  temporary  renal  irritation.  Albumin  and  formed 
elements  may  persist  for  a  time  after  the  termination  of  the  fever. 
Their  occurrence  is  explained  by  the  examination  of  renal  tissue  from 
cases  dying  from  pneumonia,  as  in  the  observations  on  45  autopsies 
by  Frankel  and  Reiche,4  who  found  pathologic  renal  changes  in  all 
but  one  of  the  cases.  These  consisted  of  changes  in  the  renal  epithe- 
lium (coagulation  necrosis  and  plasmolysis),  usually  without  involve- 
ment of  cell  nuclei.  In  some  cases  there  was  an  exudate  in  Bowman's 
capsule  at  times  with  the  presence  of  red-blood  corpuscles.  Prolifera- 
tion of  the  capsular  epithelium,  interstitial  and  vascular  changes 
were  not  observed.  In  some  of  the  cases  no  albumin  had  been  found 
in  the  urine  during  life.  Deutero-albumose  was  found  in  the  urine 
by  Krehl  and  Matthes.5    True  peptone  was  found  by  Ito.6 

The  Spleen  and  Lymph  Glands. — Enlargement  of  the  spleen  occurs  in 
pneumonia  as  in  other  acute  infections.  The  weight  exceeded  250  grams 
in  43  (34.6  per  cent.)  of  124  autopsies  on  patients  dying  with  pneu- 
monia. Eug.  Frankel  and  F.  Reiche7  found  enlargement  in  about 
40  per  cent,  of  their  fatal  cases.  Musser  and  Norris  state  that  splenic 
enlargement  occurred  clinically  in  791  (34.6  per  cent.)  of  1416  clinical 
cases,  while  Frankel8  was  able  to  establish  enlargement  in  only  15 
per  cent,  of  his  cases.  The  spleen  was  felt  in  only  3  per  cent,  of  our 
cases.  Enlargement  of  the  lymph  glands  has  not  been  noted  in  our 
cases. 

Nervous  System. — Headache  is  a  frequent  symptom  in  the  early 
stages  of  the  disease.     Severe  nervous  symptoms  are  more  common 

1  Verhandl.  d.  Naturforschergesellsch.  in  Basel,  Bd.  xiii,  p.  312,  quoted  from  Frankel. 

2  Johns  Hopkins  Hosp.  Bull.,  1902,  p.  307. 

3  Verhandl.  d.  XVI  Kongresses  f.  inn.  Med.,  Wiesbaden,  1898,  p.  507. 

4  Zeit.  f.  klin.  Med.,  Bd.  xxv,  p.  230. 

s  Deut.  Arch.  f.  klin.  Med.,  Bd.  liv,  p.  501.  «  Ibid.,  1901,  lxxi,  35. 

7  Zeit.  f.  klin.  Med.,  Bd.  xxv,  p.  230.  »  Loc.  cit.,  p.  308. 


192  DISEASES  OF   THE  LUNGS 

in  children  than  in  adults,  and  the  disease  at  times  begins  with  convul- 
sions in  place  of  an  initial  chill.  In  rare  instances,  convulsions  initiate 
the  attack  in  adults,  more  often  in  alcoholics,  epileptics,  neurotic 
individuals  and  the  insane.  Insomnia  may  be  a  troublesome  symptom. 
There  is  no  well-marked  difference  between  the  effects  on  the  nervous 
system  in  pneumonia  and  in  other  severe  acute  infections. 

Meningismus. — The  clinical  features  embraced  under  this  term 
are  also  spoken  of  as  "cerebral  pneumonia."  In  children  and  at  times 
in  adults  the  pulmonary  character  of  the  infection  may  be  masked  by 
a  predominance  of  cerebrospinal  symptoms.  There  may  be  severe 
headache,  vomiting,  irritability,  involuntary  urine  and  feces,  stiffness 
or  retraction  of  the  neck  and  spine,  increased  irritability  of  motor 
nerves  (Trousseau's  sign),  inability  to  extend  the  leg  normally  with 
the  thigh  flexed  (Kernig's  sign)  and  delirium  or  coma,  so  that  for  a 
time  the  case  may  be  regarded  as  one  of  meningitis.  Meningismus 
was  observed  in  13  of  500  cases  by  Kirchheim,1  and  in  26  of  250  children 
by  Otten.2  The  absence  of  evidence  of  organic  disease  is  important 
in  the  differentiation  of  such  cases  from  those  with  meningo-encephalitis, 
meningitis,  nephritis  and  uremia  and  otitis  media.  Paralyses  and  local- 
ized convulsive  movements  are  lacking.  The  pupils  and  eye-grounds 
are  normal.  Clear  fluid,  without  albumin  or  excess  of  formed  elements, 
is  obtained  by  lumbar  puncture.  The  spinal  fluid  was  under  increased 
tension  in  a  fewr  of  Kirchheim's  cases,  and  in  all  but  1  of  13  of  Otten's 
cases.  A  careful  daily  examination  of  the  lungs  usually  discloses  the 
pulmonary  character  of  the  infection.  The  symptoms  of  meningeal 
irritation  subside  with  or  shortly  after  the  crisis.  The  prognosis 
appears  not  to  be  unfavorably  influenced.  Meningo-encephalitis  and 
meningitis  are  considered  under  Complications. 

Delirium. — This  is  common  and  usually  toxic  in  origin.  Inanition, 
alcoholism,  and  meningitis  may  be  responsible.  Delirium  was  noted 
in  1343  (17  per  cent.)  of  7624  of  Musser  and  Norris'  collected  cases.  It 
is  more  frequent  with  extensive  pulmonary  involvement  and  is  thought 
to  be  more  common  when  the  apex  is  involved.  Heinze3  observed 
severe  nervous  symptoms  in  98  of  317  cases.  In  40.17  per  cent,  the 
pneumonia  was  apical  and  in  25  per  cent,  basal.  The  height  of  the 
temperature  is  of  moment  and  the  delirium  is  more  marked  during 
the  evening  exacerbations  of  the  fever.  The  mortality  is  higher  in 
those  with  than  in  those  without  delirium.  Delirium  may  be  an 
initial  symptom,  but  is  more  common  and  more  marked  at  the  height 
of  the  disease.  There  may  be  only  a  mild,  dreamy  incoherence,  a 
low  muttering  confusion  or  a  more  excited  state  with  hallucinations, 
delusions  of  various  sorts,  and  in  rare  instances  acute  mania.  Homi- 
cidal or  suicidal  tendency  may  be  present.  The  onset  may  be  sudden 
and   unexpected,   and   nurses   and   attendants   should   be   cautioned 

1  Med.  Klinik,  1908,  No.  38,  p.  1461. 

2  Jahrb.  f.  Kinclerh.,  1909,  N.  F.,  69,  p.  568. 

3  Arch.  d.  Heilk.,  1868,  Bd.  ix,  p.  49. 


LOBAR  PNEUMONIA  193 

against  leaving  patients  with  pneumonia  alone,  lest  they  injure  them- 
selves or  others.  Postcritical  delirium  is  occasionally  observed,  and 
is  usually  but  not  always  associated  with  manifestations  of  exhaus- 
tion. Pohlmann1  noted  delirium  with  or  after  the  crisis  in  6  of  239 
cases.  Two  of  the  six  died.  Eisner2  reports  4  cases  of  postcritical 
delirium,  occurring  from  three  to  ten  days  after  defervescence.  All 
recovered.  Postpneumonic  psychoses  are  usually  of  short  duration, 
but  may  last  for  weeks  or  months.  According  to  Krafft-Ebing,3 
recovery  occurs  in  84  per  cent,  of  the  cases.  In  some  cases  the  condi- 
tion passes  into  dementia.  Pneumonia  is  likely  to  precipitate  delirium 
tremens  in  alcoholics.  The  mortality  is  high.  Of  357  cases  of  pneu- 
monia with  delirium  tremens  in  Musser  and  Norris'  series,  132  (36 
per  cent.)  died. 

Digestive  System. — The  tongue  may  be  coated  and  the  whole  mouth 
and  lips  may  be  dry.  The  appetite  may  be  lost.  Vomiting  is  frequent, 
especially  in  children.  Of  5047  cases  collected  by  Musser  and  Norris 
vomiting  occurred  in  1356  (26.8  per  cent.) ;  nausea  in  134  (13.5  per  cent.) 
of  991  cases.  Vomiting  may  be  troublesome  from  irritation  of  the 
pharynx  by  the  expectoration.  Constipation  is  more  common  than 
diarrhea.  Intestinal  flatus  may  be  present  and  aggravate  the  dyspnea. 
It  may  be  due  to  restricted  movement  of  the  diaphragm  or  toxic 
paresis  of  the  intestine.    Jaundice  is  considered  under  Complications. 

Delayed  Resolution. — Frankel4  observed  an  absence  of  resolution 
in  63  (6.3  per  cent.)  among  about  1000  cases  of  pneumonia.  Musser 
and  Norris  found  delayed  resolution  reported  in  105  (4.1  per  cent.) 
among  2548  cases.  Flexner5  and  others  (see  Autolysis,  p:  180)  have 
found  that  in  the  stage  of  gray  hepatization,  autolysis  takes  place 
quickly  and  perfectly,  while  in  the  stage  of  red  hepatization  it  is  very 
imperfect,  a  fact  which  is  attributed  to  the  small  number  of  pus  cells 
present  in  the  latter  condition.  It  is  also  found  that  if  the  lung  in 
unresolved  pneumonia  is  exposed  to  conditions  favoring  autolysis, 
the  process  is  slow  and  incomplete  as  compared  with  what  takes  place 
in  gray  hepatization.  The  failure  to  resolve  is  due  to  organization 
of  the  exudate  and  replacement  by  connective  tissue,  as  is  shown 
by  postmortem  examination,  but  the  underlying  factors  are  not  yet 
clear,  although  Opie's6  observations  on  enzymes  and  antienzymes 
of  inflammatory  exudates  may  have  a  bearing  on  this  question.  He 
noted  that  the  serum  of  an  inflammatory  exudate  has  the  power  of 
inhibiting  the  action  of  proteolytic  ferments  contained  in  the  leuko- 
cytes, this  antienzymatic  power  being  possessed  by  the  blood-serum 
from  which  it  doubtless  passes  into  the  exudate.  Frankel  regards 
a  delay  of  resolution  beyond  three  weeks  as  evidence  of  developing 

1  Statistische  und  klin.  Beobachtungen  iiber  die  genuine  kr.  Pneum.,  1888,  8°, 
Erlangen,  p.   50. 

2  Med.  News,  New  York,  January  8,  1898,  p.  33. 

3  Lehrb.  d.  Psychiatrie,  5  Aufl.,  Stuttgart,  1893,  p.  191.  4  Loc.  cit.,  p.  337. 

5  Trans.  Assoc.  Amer.  Phys.,  1903,  xviii,  359. 

6  Jour.  Exp.  Med.,  1905,  vii,  316. 

13 


194  DISEASES  OF  THE  LUNGS 

pulmonary  induration,  provided  such  other  complications  as  abscess, 
etc.,  can  be  excluded.  That  so  long  an  interval  is  unnecessary  in  excep- 
tional instances  is  shown  by  the  finding  of  organizing  pneumonia 
at  autopsy  in  6  cases  at  the  Massachusetts  General  Hospital  within 
from  seven  to  seventeen  days  of  the  onset  of  acute  pulmonary  symp- 
toms, as  noted  in  the  section  on  Subacute  and  Chronic  Indurative 
Pneumonia.  Pulmonary  tuberculosis,  empyema,  abscess  and  gangrene 
must  be  excluded  before  the  diagnosis  of  delayed  resolution  is  made. 

Clinical  Varieties  of  Pneumonia. — Certain  types  of  pneumonia 
(litter  sufficiently  from  the  ordinary  forms  to  deserve  special  mention. 

Central  Pneumonia. — The  solidification  may  begin  at  any  part  of  the 
lung.  If  it  begins  at  the  root  and  spreads  slowly  toward  the  periphery, 
physical  signs  may  be  lacking  for  several  days.  In  some  instances  the 
lungs  are  negative  throughout.  Other  features,  however,  usually 
permit  of  a  diagnosis.  The  acute  onset  with  chill,  rusty  sputum, 
increase  in  the  rate  of  respiration  and  leukocytosis  are  important 
signs.  In  rare  instances  the  diagnosis  may  be  in  doubt  until  crisis 
occurs. 

Massive  Pneumonia. — In  rare  instances  the  bronchi  of  the  involved 
region  may  be  filled  with  fibrinous  exudate.  There  may  then  be 
flatness  on  percussion,  diminished  or  absent  respiratory  murmur, 
voice  sounds,  whisper  and  tactile  fremitus.  If  the  lower  part  or  the 
whole  of  one  lung  is  involved,  pleurisy  with  effusion  may  be  simulated. 
If  the  patient  is  asked  to  cough,  fibrinous  plugs  may  be  expelled  from 
the  bronchi  and  the  signs  of  solidification  appear.  Absence  of  Grocco's 
paravertebral  triangle  and  the  maintenance  of  the  heart  in  a  normal 
position  are  against  an  effusion.  A  zone  of  relative  resonance  in  the 
paravertebral  region  on  the  affected  side  is  in  favor  of  pneumonia. 
A  resort  to  exploratory  puncture  may  be  necessary  to  settle  the 
diagnosis. 

Migratory  Pneumonia. — In  a  small  number  of  cases,  the  pneumonia 
may  spread  from  one  lobe  to  another,  resolution  going  on  in  one  place 
while  the  infiltration  progresses  in  another.  In  this  way  all  the  lobes 
of  one  or  both  lungs  may  be  successively  involved.  In  some  instances 
a  lobe  previously  attacked  may  be  reinfected.  From  its  character, 
such  a  course  has  been  termed  erysipelatous.  The  cases  are  likely 
to  be  protracted  and  severe.  The  spread  may  take  place  by  continuity 
and  to  such  cases  the  term  migratory  pneumonia  is  more  strictly 
applicable.  In  some  degree  many  pneumonias  belong  to  this  group, 
as  is  shown  by  the  frequency  with  which  at  autopsy  an  extension  is 
observed  from  one  to  a  neighboring  or  another  lobe. 

Asthenic  or  Senile  Pneumonia. — This  form  has  also  been  termed 
"typhoid  pneumonia,"  adynamic,  putrid  or  pythogenic  pneumonia, 
and  is  characterized  by  an  extreme  degree  of  prostration.  It  is  more 
common  in  the  aged  and  in  those  enfeebled  by  chronic  disease.  The  diag- 
nosis may  remain  for  some  days  in  doubt.  The  term  typhoid  pneumonia 
is  unfortunate,  as  it  suggests  a  form  of  the  disease  due  to  the  typhoid 


LOBAR  PNEUMONIA  195 

bacillus,  which  rarely  if  ever  occurs.  When  pneumonia  complicates 
typhoid,  it  is  usually  due  to  other  organisms  than  the  typhoid  bacillus. 
The  onset  of  asthenic  pneumonia  is  usually  insidious  and  without 
an  initial  chill.  There  may  be  intense  nervous  symptoms  such  as 
stupor  or  delirium.  Such  gastro-intestinal  symptoms  as  vomiting, 
diarrhea  and  meteorism  may  be  prominent  features  and  distract 
attention  from  the  lung  to  the  alimentary  canal.  Cough  may  be 
absent.  Cardiac  weakness  may  be  a  prominent  feature.  If  pulmonary 
signs  are  doubtful  or  absent,  typhoid  may  be  closely  simulated.  The 
absence  of  rose  spots  and  enlargement  of  the  spleen,  negative  blood-cul- 
tures and  agglutinative  tests  for  typhoid  and  paratyphoid,  positive  blood- 
cultures  for  pneumococci  and  leukocytosis  may  permit  of  the  diagnosis 
of  a  pneumococcus  infection.  The  course  of  such  cases  is  likely  to  be 
protracted.  Varying  grades  of  jaundice  may  be  present.  The  tempera- 
ture is  usually  not  high  and  may  be  unelevated.  Defervescence  is 
more  often  by  lysis  than  crisis.  Leichtenstern1  states  that  a  termina- 
tion in  abscess  and  gangrene  is  not  infrequent.  Frankel2  believes  that 
in  spite  of  their  atypical  course,  the  majority  of  cases  of  asthenic 
pneumonia  are  due  to  infection  with  true  pneumococci.  Heightened 
virulence  of  the  organism,  diminished  resistance  of  the  host  or  both 
may  be  responsible. 

Pneumonia  in  Children. — Croupous  pneumonia  is  relatively  infrequent 
before  the  second  year.  The  disease  in  children  is  likely  to  differ  from 
the  type  seen  in  adults.  The  initial  chill  is  less  common  and  is  likely 
to  be  replaced  by  such  nervous  symptoms  as  convulsions,  delirium 
or  stupor.  Gastro-intestinal  disturbances,  as  nausea  and  vomiting, 
are  likely  to  be  more  prominent  features.  Cough  is  usually  present 
but  is  rarely  distressing.  Expectoration  is  not  common  under  five 
years  of  age.  The  temperature  is  likely  to  be  more  elevated  and  the 
pulse  proportionally  higher  than  in  adults.  The  physical  signs  may 
appear  later  in  the  course  of  the  disease  and  the  diagnosis  may  be  in 
doubt  for  some  days.  An  expiratory  grunt,  with  fever  of  an  acute 
onset,  leukocytosis  and  rapid  respiration  out  of  proportion  to  the 
elevation  of  the  pulse  may  be  the  only  suggestive  signs.  The  leuko- 
cytosis is  more  constant  and  in  general  higher  than  in  adults.  The 
knee-jerks  may  be  diminished  or  absent.  The  course  of  the  disease  is 
more  favorable.  Among  1482  cases  collected  by  Holt,3  death  occurred 
in  only  60  (4  per  cent.).  A  fatal  result  is  usually  due  to  extensive 
disease  or  to  complications.  Delayed  resolution  is  less  common, 
empyema  and  otitis  media  more  common  than  in  adults.  According 
to  Frankel4  transient  irregular  heart  action  is  not  uncommon  after 
the  fall  of  the  fever. 

Apical  Pneumonia. — The  right  apex  is  much  more  frequently  affected 
than  the  left.     Stupor  and  delirium,  hyperpyrexia  and  pericarditis 

1  Ueber  asthenische  Pneumonien,  Volkmann's  Samml.  klin.  Vortrage,  1874,  No.  82. 

2  Loc.  cit.,  p.  320.  3  Diseases  of  Infancy  and  Childhood,  1903. 
4  Loc.  cit.,  p.  323. 


196  DISEASES  OF  THE  LUNGS 

are  said  to  be  more  common  in  pneumonia  of  the  apex  than  at  other 
parts  of  the  lung,  but  this  is  not  confirmed  by  my  cases. 

Terminal  Pneumonia. — Pneumonia  is  a  frequent  termination  of  chronic 
diseases,  such  as  arteriosclerosis,  chronic  heart  lesions,  kidney  disease 
and  diabetes,  as  is  shown  by  autopsy  records.  The  initial  chill  and 
pain  in  the  side  are  often  lacking.  Sputum  may  be  absent.  Fever 
may  be  slight  or  absent.    The  disease  may  be  unsuspected  during  life. 

Pneumonia  in  Alcoholics. — As  in  the  aged,  croupous  pneumonia  in 
alcoholics  is  likely  to  be  of  the  asthenic  type  and  to  run  an  atypical 
course.  Marked  nervous  symptoms  are  usually  present  and  of  the 
type  usually  seen  in  delirium  tremens.  Unless  the  lungs  are  carefully 
examined,  the  pneumonia  may  readily  be  overlooked.  The  mortality 
is  high. 

Pneumonia  in  Pregnancy. — Pneumonia  appears  to  be  infrequent  in 
pregnancy.  Among  13,611  cases  of  pregnancy  collected  by  Musser  and 
Xorris  there  were  only  120  instances  of  pneumonia  (0.8  per  cent.). 
The  disease  is  likely  to  run  a  severe  course  and  often  leads  to  abortion. 
The  frequency  of  abortion  and  the  maternal  mortality  increase  with 
the  advancement  of  pregnancy.  Of  the  infants  who  have  reached  a 
viable  age,  a  large  proportion  die.  Aufrecht1  believes  that  abortion 
is  produced  by  infection  of  the  placental  site  with  pneumococci.  Some 
caution  must  be  observed  in  the  diagnosis  of  pneumonia  in  cases  of 
abortion.  Pulmonary  embolism  and  infarction  are  more  common  than 
pneumonia  in  lying-in  women  and  the  clinical  features  may  closely 
simulate  pneumonia. 

Postoperative  and  Ether  Pneumonia.- — In  a  collected  series  of  139,101 
cases  of  anesthesia,  Musser  and  Norris  found  pneumonia  in  499 
(0.35  per  cent.).  Postoperative  pneumonias  are  usually  lobular  in  type 
and  are  considered  more  fully  in  the  section  on  Bronchopneumonia. 

Abortive  Pneumonia. — In  rare  instances,  the  course  of  the  disease 
may  be  very  short.  Leube,2  Weil,3  and  Bernhardt4  each  report  the 
unusual  occurrence  of  a  typical  pneumonia  of  one  day  in  duration. 
Bechtold5  found  10  cases  occurring  close  together  in  one  ward  at  the 
Wiirtzburg  clinic.  Cases  in  which  from  one  to  three  days  elapse  from 
the  beginning  of  symptoms  to  the  fall  of  the  fever  may  also  be  classed  in 
this  group.  Pneumonias  of  two  days'  to  three  days'  duration,  although 
unusual,  are  occasionally  seen.  One  case  of  two  days'  and  a  second  of 
three  days'  duration  occurred  among  200  cases  at  the  Massachusetts 
General  Hospital. 

Pneumonia  and  Other  Diseases. — Pulmonary  Tuberculosis. — Croup- 
ous pneumonia  as  a  complication  of  pulmonary  tuberculosis  is  rare. 
The  diagnosis  in  a  tuberculous  subject  must  be  made  with  caution 

1  Nothnagel's  Practice,  Disease  of  the  Bronchi,  Pleura,  and  Lungs,  American  edition, 
p.  501. 

2  Thuringer  arztl.  KorrespondenzbL,  April,  1877. 

»  Berl.  klin.  Woch.,  1879,  No.  45,  p.  665.  «  Zeit.  f.  klin.  Med.,  Bd.  i,  p.  630. 

''  Munch,  med.  Woch.,  1905,  No.  44,  vol.  Hi. 


LOBAR  PNEUMONIA  197 

lest  the  subacute  forms  of  pulmonary  tuberculosis  or  acute  pneumonic 
phthisis  be  mistaken  for  croupous  pneumonia.  Of  750  cases  of  pneu- 
monia observed  by  Friinkel,1  only  15  (2  per  cent.)  showed  coincident 
and  clinically  recognizable  pulmonary  tuberculosis.  Scllo2  reports 
that  of  these  15  cases,  5  terminated  by  lysis  and  3  by  crisis,  while  7 
died.  Huss3  reported  36  cases  of  which  one-third  died.  A  family 
history  of  the  disease  or  opportunity  for  contagion,  previous  history 
of  phlyctenular  conjunctivitis,  fistula  in  ano,  cervical  adenitis,  primary 
pleurisy,  hemoptysis  out  of  a  clear  sky,  or  cough  and  failing  health 
may  be  suggestive  features.  Signs  of  apical  disease  may  be  obtained 
on  physical  examination  or  with  the  .r-ray,  and  tubercle  bacilli  may  be 
found  in  the  expectoration.  The  ultimate  effect  on  pulmonary  tuber- 
culosis of  lobar  pneumonia  from  which  the  patient  recovers  is  little 
known.  In  some  instances  the  pneumonia  appears  to  have  little  influ- 
ence on  the  tuberculous  process,  in  others  the  tuberculosis  progresses 
more  rapidly  or  miliary  tuberculosis  follows. 

Pneumonia  Complicating  Heart  and  Renal  Disease. — The  disease  is 
likely  to  present  atypical  features  in  cases  of  cardiac  disease  with 
broken  compensation  and  in  advanced  renal  disease.  An  initial 
chill  is  often  lacking  and  the  temperature  may  be  little  or  not  at 
all  elevated.  A  differentiation  between  pneumonia  and  pulmonary 
infarction  may  be  impossible.  In  some  cases  the  two  conditions 
coexist.  The  sputum  may  be  rusty  or  contain  pure  blood.  It  is 
usually  abundant,  frothy,  and  less  tenacious  than  in  pneumonia 
uncomplicated  by  passive  congestion.  The  mortality  is  high  and  at 
autopsy  the  hemorrhagic  character  of  the  exudate  may  be  a  striking 
feature. 

Pneumonia  and  Diabetes. — Pneumonia  complicating  diabetes  usually 
runs  an  atypical  and  severe  course.  It  may  terminate  in  gangrene. 
Cases  ending  fatally  commonly  die  in  coma.  As  in  other  febrile  com- 
plications of  diabetes,  the  glycosuria  is  likely  to  diminish  and  may 
disappear.  Pneumonia  occurred  as  a  complication  in  6  (1  per  cent.) 
among  530  cases  of  diabetes  at  the  Massachusetts  General  Hospital. 
The  onset  was  sudden  with  the  usual,  acute  symptoms  in  four.  In 
two  the  onset  was  insidious.  The  temperature  was  elevated  in  five, 
subnormal  in  the  remaining  case.  Leukocytosis  was  present  (between 
14,000  and  21,000)  in  five.  The  white  cells  numbered  only  8000  in 
one  case.  The  pneumonia  was  fatal  in  all.  Four  of  the  six  patients 
died  in  coma. 

Pneumonia  and  Typhoid  Fever. — Lobar  is  less  common  than  broncho- 
pneumonia in  typhoid  fever.  Among  3514  cases  of  pneumonia  col- 
lected by  Musser  and  Norris,  were  56  cases  of  typhoid  fever  with  26 
deaths  (42.8  per  cent.).  Among  2579  cases  of  typhoid  fever  at  the 
Massachusetts  General  Hospital  (1897  to  1913)  were  13  cases  of 
lobar   pneumonia  with  9   deaths    (69  per  cent.)     There   are  three 

1  Loc.  cit.  2  Zeit.  f.  klin.  Med.,  Bd.  xxxvi,  p.  112. 

3  Quoted  from  Musser  and  Norris,  Osier.     Mod.  Med.,  1907,  ii,  550. 


198 


DISEASES  OF   THE  LUNGS 


groups  of  cases:  (1)  In  the  first  group,  the  lobar  pneumonia  occurs 
early  in  the  course  of  the  typhoid  and  there  may  then  he  an  initial 
chill,  pain  in  the  side,  and  cough  with  rusty  sputum.  Crisis  may  follow 
with  subsequent  elevation  of  temperature,  hut  more  commonly  the 
fever  persists  beyond  the  period  of  its  expected  decline  and  the  pro- 
longation of  the  illness  may  be  the  first  intimation  of  the  presence  of 
typhoid.  Pneumonia  occurring  at  the  onset  of  typhoid  fever  was 
observed  in  3  of  22  cases  by  McCrae,1  but  in  none  of  this  series.  (2) 
In  the  second  group,  the  pneumonia  occurs  while  the  typhoid  fever 
is  at  its  height  after  the  second  week  of  the  illness,  and  its  clinical 
features  are  then  so  masked  as  to  make  the  diagnosis  difficult.    Chill, 

Fig.  30 


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Tj'phoid  fever  followed  by  lobar  pneumonia,  beginning  on  the  fifth  day  of 
convalescence.     (567-200.) 

pain,  cough  and  expectoration  may  be  absent  and  the  pneumonia 
may  be  suggested  only  by  an  elevation  of  the  rate  of  respiration  and 
pulse  and  cyanosis.  If  the  patient  is  not  severely  toxic,  one  or  more 
of  these  symptoms  may  be  present.  The  temperature  is  usually 
little  changed.  An  onset  during  the  course  of  the  disease  occurred 
in  19  of  McCrae's  22  cases  and  in  10  of  13  in  this  series.  Of  the  10 
cases  8  died.  A  leukocyte  count  was  done  during  the  pneumonia  in 
5  of  the  10  cases.  In  3  cases  there  was  no  leukocytosis.  In  the  two 
remaining  cases  the  leukocytes  rose  from  3700  during  the  typhoid  to 
7400  during  the  pneumonia  in  one  and  from  4500  during  the  typhoid 


i  Osier.    Mod.  Med.,  vol.  i,  p.  122. 


LOBAR  PNEUMONIA 


199 


Fig.  31 


to  13,000  during  the  pneumonia  in  the  second.  (3)  In  a  third  group, 
the  pneumonia  occurs  during  convalescence  and  its  recognition  then  pre- 
sents no  special  difficulty.  Three  such  cases  were  present  in  this  series. 
In  one  (Fig.  30),  the  pneumonia  began  on  the  fifth  day  of  convalescence 
and  ran  a  typical  course  with  crisis  on  the  eighth  day.  The  white  count 
rose  from  2000  during  the  typhoid  to  10,000  during  the  pneumonia. 
In  the  second  case,  a  typhoid  of  four  weeks'  duration  was  followed  by  a 
relapse  of  two  to  three  weeks  and  pneumonia  beginning  on  the  tenth 
day  of  convalescence.  The  white  count  was  3800  during  the  typhoid 
and  rose  to  10,000  during  the  pneumonia,  from  which  the  patient 
recovered.  In  the  third  case,  the  pneumonia 
occurred  after  two  days  of  normal  tempera- 
ture and  proved  fatal. 

When  pneumonia  occurs  at  the  height  of 
the  typhoid  fever  the  diagnosis  may  be  very 
puzzling.  It  is  difficult  to  differentiate  lobar 
pneumonia  from  bronchopneumonia,  which  is 
a  more  common  complication.  Pulmonary 
embolism  and  infarction  may  present  prac- 
tically identical  clinical  features,  and  if,  as 
not  infrequently  happens,  evidence  of  venous 
thrombosis  in  the  peripheral  veins  is  absent, 
the  diagnosis  may  be  impossible  for  a  time. 
In  one  case  of  typhoid  fever,  pulmonary 
embolism  was  mistaken  for  pneumonia  until 
four  days  later,  when  a  phlebitis  of  the  leg 
first  became  manifest.  If  the  pain  of  pleural 
involvement  in  pneumonia  complicating  ty- 
phoid fever  is  referred  to  the  abdomen,  intes- 
tinal perforation  may  be  simulated.  In  one 
case,  a  sudden  drop  in  the  temperature  to  nor- 
mal, rapid  elevation  of  the  pulse  and  rigidity 
of  the  abdomen  in  the  third  week  of  typhoid 
suggested  perforation  which  was  not  confirmed 
at  operation.  The  signs  of  pneumonia  de- 
veloped the  next  day  and  the  patient  died. 

Pneumonia  and  Malaria. — Lobar  pneumonia  may  complicate  any 
form  of  malaria.  When  it  occurs  in  the  course  of  the  estivo-autumnal 
infection  it  is  very  fatal.  There  is  no  evidence  that  the  malarial 
parasite  can  cause  true  pneumonia.  The  typical  fever  curve  of  malaria 
is  usually  masked  by  the  elevation  from  the  pneumonia.  The  fever 
curve  of  uncomplicated  pneumonia  may  resemble  that  of  intermittent 
fever  (Fig.  31). 

Pneumonia  and  Insanity. — According  to  Krafft-Ebing1  pneumonia 
is  the  cause  of  death  in  a  sixth  of  the  cases.    The  pneumonia  is  likely 


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(703-55.) 


1  Lehrbuch  d.  Psychiatrie,  5  Aufl.,  Stuttgart,  1893,  p.  234. 


200  DISEASES  OF   THE  LUNGS 

to  be  latent  without  chill,  cough  or  sputum  and  discovered  only  on 
physical  examination. 

Physical  Signs.  —Inspection. — Herpes  and  cyanosis  of  the  lips,  the 
inspiratory  dilatation  of  the  ahe  nasi,  the  rapid  respiration  and  the 
use  of  the  accessory  muscles  in  breathing  give  important  indications 
of  the  presence  of  pneumonia.  The  patient  usually  lies  on  the  back, 
at  times  more  comfortably  on  the  affected  side,  thus  allowing  the  sound 
lung  full  play  and  diminishing  the  pain  by  limiting  the  motion  of  the 
inflamed  pleurae.  Orthopnea  is  rare.  Unequal  expansion  of  the  two 
sides  of  the  chest  may  indicate  the  lung  affected,  a  greater  excursion 
being  observed  on  the  unaffected  side.  When  the  disease  is  in  the  lower 
lobe,  the  upper  region  of  the  chest  on  the  same  side  may  show  increased 
inspiratory  motion.  Diminished  amplitude  of  the  diaphragm  shadow 
may  be  noted  on  the  affected  side.  But  the  diminished  excursion  of  the 
affected  lung  is  less  marked  with  pneumonia  than  with  pleural  effusion. 
Pulsation  of  the  involved  part  of  the  lung  synchronous  with  cardiac 
systole  may  be  seen  in  some  cases. 

Palpation,. — Variation  in  the  relative  expansion  of  the  two  sides  of 
the  chest  may  be  better  felt  than  seen.  Pleural  friction  and  coarse 
rales  may  at  times  be  palpated.  The  tactile  fremitus  is  usually 
increased  and  becomes  more  marked  with  the  progress  of  the  infiltra- 
tion. If  the  pleura  is  much  thickened,  however,  it  may  be  diminished. 
If  the  bronchi  are  filled  with  tenacious  secretion  or  fibrinous  exudate 
(massive  pneumonia),  the  tactile  fremitus  may  be  diminished  or  absent. 
Removal  of  the  bronchial  obstruction  by  cough  may  be  followed  by 
reappearance  of  the  fremitus.  In  women  and  children,  owing  to  the 
high  pitch  of  the  voice,  the  tactile  fremitus  may  be  of  little  or  no  value. 
In  central  pneumonia  the  tactile  fremitus  may  be  unchanged.  A 
perceptible  increase  in  the  temperature  of  the  skin  overlying  the  site 
of  the  pneumonia  may  be  appreciated. 

Percussion. — Both  light  and  strong  percussion  should  be  used,  the 
former  at  times  making  evident  a  dulness  dependent  on  superficial 
and  the  latter  that  due  to  deep  infiltration  of  the  pulmonary  tissue. 
During  the  stage  of  engorgement  the  percussion  note  is  relatively 
dulled  or  dull;  at  times  it  has  a  tympanitic  quality  (Skoda's  resonance). 
This  tympanitic  quality  is  more  commonly  observed  when  the  aepx 
is  involved.  Its  cause  is  not  clear.  It  may  be  due  to  the  relaxation 
of  alveolar  spaces  which  still  contain  air  or,  as  seems  more  likely,-  to 
the  transmission  of  the  percussion  impact  through  solid  lung  to  the 
air  contained  in  the  bronchi  and  trachea.  At  times  a  change  in  the 
tympanitic  quality  is  observed  with  the  mouth  open  and  closed 
(William's  tracheal  tone).  In  involvement  of  the  low7er  lobes,  tympany 
may  be  due  to  proximity  of  the  stomach.  A  cracked-pot  note  may  be 
present  when  pulmonary  solidification  surrounds  a  large  bronchus. 

In  the  stage  of  red  hepatization  the  degree  of  dulness  varies.  The 
note  may  be  flat,  but  there  is  not  the  total  absence  of  resonance  and 
the  sense  of  resistance  to  the  finger  found  in  large  effusions.    The  extent 


LOBAR  PNEUMONIA  201 

of  the  dulness  varies.  It  is  often  limited  to  a  part  of  a  lobe  and  all 
parts  of  the  lung  should  be  carefully  investigated,  not  forgetting  to 
percuss  the  upper  parts  of  the  axillary  region.  In  other  cases,  one  lung 
may  be  dull  throughout,  and  the  limits  of  the  dulness  may  then  exceed 
the  normal  boundaries  from  swelling  of  the  pulmonary  tissue.  When 
the  consolidation  involves  the  inferior  lobe  and  is  of  considerable 
extent,  a  zone  of  relative  resonance  may  be  determined  in  the  para- 
vertebral region  on  the  affected  side.1  This  is  probably  due  to  increased 
spinal  resonance  from  compensatory  emphysema  of  the  unaffected 
lung. 

In  central  pneumonia  only  slight  impairment  of  the  percussion  note 
may  be  determined  over  the  site  of  the  involvement.  In  some  cases 
there  may  be  no  change  on  percussion  throughout  the  course  of  the 
disease.  Compensatory  emphysema  over  an  involved  region  may  so 
mask  the  dulness  from  underlying  infiltration  as  to  make  it  undetect- 
able. Hyperresonance  over  neighboring  parts  of  the  same  or  the 
whole  of  the  other  lung  can  often  be  demonstrated. 

Auscultation.— All  parts  of  the  lungs  should  be  carefully  covered 
with  the  stethoscope.  The  signs  on  auscultation  are  very  variable  in 
different  cases.  The  finding  of  rales  persistently  present  at  one  place 
in  the  lung  during  repeated  examinations  may  in  rare  instances  be  the 
only  auscultatory  sign.  In  the  early  stages  of  the  disease,  fine,  conso- 
nating,  moist  rales  (crepitant  rales)  are  commonly  heard.  They  are 
usually  heard  toward  the  end  of  inspiration  or  forced  inspiration  as 
a  succession  of  minute  crackling  sounds,  and  are  probably  due  to  a 
disturbance  by  the  incoming  air  of  the  sticky  exudate  in  the  finest 
branches  of  the  bronchi.  They  have  also  been  thought  to  be  pleural 
in  origin.  The  crepitant  rales  in  pneumonia  are  to  be  distinguished 
by  their  clear-cut,  sharp  and  distinct  or  resonating  (consonating) 
quality  from  non-consonating  rales  arising  in  bronchi  in  cases  in  which 
there  is  no  consolidation  of  the  surrounding  pulmonary  tissue.  The 
distinction  is  not  always  easily  made,  but  is  of  value  in  differentiating 
consolidation  from  simple  bronchitis,  hypostatic  congestion  and  edema. 
Crepitant  rales  often  disappear  during  the  stage  of  red  hepatization, 
to  reappear  during  resolution — redux  crepitus.  If  bronchitis  of  the 
larger  tubes  coexists,  coarser  rales  may  mask  them. 

Suppression  of  the  breathing  is  usually  one  of  the  first  signs  of 
pneumonia.  During  the  first  twenty-four  hours  after  the  chill,  slight 
dulness  on  percussion,  diminished  vesicular  breathing  and  crepitant 
rales  are  often  the  only  local  manifestations.  In  some  cases  with  the 
suppression  of  the  breathing  there  is  a  change  in  its  quality,  the  expira- 
tion being  somewhat  longer  and  of  a  higher  pitch  than  over  a  corre- 
sponding place  in  the  opposite  lung.  As  the  disease  progresses,  the 
breathing  usually  becomes  more  and  more  intense,  with  loud  and  high- 

1  F.  T.  Lord,  Percussion  of  the  Paravertebral  Region  on  the  Affected  Side  in  the 
Differentiation  of  Pneumonia  and  Pleurisy  with  Effusion.  Boston  Med.  and  Surg. 
Jour.,  February  12,  1914. 


202  DISEASES  OF  THE  LUNGS 

pitched  inspiration  and  markedly  long,  loud  and  high-pitched  expira- 
tion. In  no  other  disease  does  bronchial  breathing  reach  such  a  degree 
of  intensity  as  in  croupous  pneumonia,  due  to  the  propagation  of  laryn- 
geal and  tracheal  sounds  through  the  solid  lung.  If  the  pleura  is  much 
thickened  or  the  bronchi  are  plugged  (massive  pneumonia),  the  breath 
sounds,  as  well  as  the  tactile  fremitus,  may  be  much  diminished  or 
absent.  If  the  bronchial  obstruction  can  be  relieved  by  cough,  bron- 
chial breathing  may  be  made  to  appear.  When  the  pneumonia  involves 
the  lung  near  the  spine,  the  breathing  may  be  bronchial  over  the 
neighboring  part  of  the  opposite  lung. 

The  spoken  voice  is  usually  loud  and  high-pitched  (bronchophony) 
over  the  consolidated  region,  and  words  may  be  more  plainly  dis- 
tinguished than  over  unaffected  parts  of  the  lung.  This  is  probably 
due  to  the  more  intense  conduction  through  the  solid  tissue.  A  short 
interval  of  bronchial  expiration  usually  follows  the  spoken  voice. 
Bronchophony  is  more  marked  in  men  than  in  women  or  children  owing 
to  the  deeper  pitch  of  the  voice  in  the  former.  It  may  be  absent  in 
massive  pneumonia.  At  times  the  voice  has  a  peculiar  bleating  or 
nasal  quality  and  is  then  spoken  of  as  aegophony.  Increase  in  the  inten- 
sity of  the  whisper  is  usually  associated  with  bronchophony. 

From  Conner  and  Dodge's1  study  of  392  cases  of  pneumonia  for  the 
purpose  of  determining  the  relative  value  of  various  physical  signs 
in  the  early  stages  of  the  disease,  they  tabulate  the  following  findings 
in  the  order  of  their. importance:  (1)  a  circumscribed  area  of  feeble 
and  indistinct  breathing;  (2)  circumscribed  impairment  without  or 
with  a  tympanitic  quality  (sitting  up);  (3)  crepitant  rales;  (4)  slight 
increase  in  intensity  and  clearness  of  the  vocal  resonance.  In  doubtful 
cases  it  is  necessary  to  test  all  the  different  signs.  Considerable  varia- 
tion in  the  findings  on  physical  examination  is  noted  in  different  cases 
and  in  the  examination  of  the  same  case  from  day  to  day. 

Signs  of  solidification,  dulness,  bronchial  breathing,  increase  of  voice, 
whisper  and  tactile  fremitus  usually  persist  for  a  fewT  days  to  a  week 
after  the  crisis  has  occurred.  In  rare  instances  they  may  last  for  weeks 
or  months.  It  is  rarely  possible,  however,  to  demonstrate  abnormal 
findings  in  uncomplicated  cases  wmich  have  fully  recovered. 

X-ray  Examination. — Fluoroscopic  or  radioscopic  examination  is  of 
value  in  indicating  the  site,  extent  and  character  of  the  pneumonic 
process.  The  radiograph  is  to  be  preferred  from  the  permanence  of 
the  record  and  the  opportunity  for  comparison  of  the  findings  at  dif- 
ferent periods  of  the  illness.  In  most  cases,  .r-ray  examination  merely 
serves  to  confirm  the  results  of  physical  examination,  but  may  dem- 
onstrate a  central  lesion  or  multiple  areas  not  apparent  on  physical 
examination;  or  assist  in  the  early  detection  of  pleural  effusion.  The 
shadow  caused  by  lobar  pneumonia  is  uneven  in  density  and  mottled 
with  ill-defined  boundaries  which  fade  out  into  the  neighboring  and 

1  Amer.  Jour.  Med.  Sci.,  September,  1903. 


LOBAR  PNEUMONIA 


203 


uninvolved  parts  of  the  lung.  An  apical,  central  or  marginal  position 
and  the  presence  of  an  uninvolved  zone  between  the  inferior  limits  of 
the  shadow  and  the  base  of  the  lung  may  be  of  importance  in  suggesting 
the  pneumonic  character  of  the  process.  Absence  of  depression  of  the 
diaphragm  and  dislocation  of  the  heart  is  also  significant.  The  shadow- 
caused  by  lobar  pneumonia  cannot  usually  be  distinguished  from  that 
due  to  thick  pleura,  confluent  bronchopneumonia  or  atelectasis. 
Pleural  effusion  presents  a  more  dense,  uniform  and  sharply  outlined 
shadow  with  curved  upper  border.  The  shadow  occupies  the  lower 
parts  of  the  pleural  space,  and  is  often  associated  with  depression  of  the 
diaphragm  and  dislocation  of  the  heart.  The  shadow  from  tumor 
is  more  dense  than  that  with  lobar  pneumonia  and  more  sharply 
outlined.     According  to  v.  Jaksch  and  Rotsky1  the  shadow  caused 

Fig.  32 


Lobar  pneumonia  of  left  lung.      (v.  Jaksch  and  Rotsky.) 

by  a  developing  infiltration  may  be  seen  to  extend  in  the  form  of  band- 
or  strip-like  shadows  from  an  initial  small  area,  but  is  more  commonly 
more  even  and  diffuse.  Resolution  may  be  observed  to  take  place 
in  the  central  parts  and  extend  eccentrically  toward  the  periphery  or, 
as  is  more  often  the  case,  in  several  places  at  the  same  time  and  more 
diffusely.  Signs  of  beginning  resolution  may  be  observed  in  the  radio- 
graph at  a  time  when  neither  the  physical  findings  nor  the  course  of 
the  fever  indicate  the  proximity  of  the  crisis.  The  picture  may 
change  in  the  course  of  twenty-four  hours.  Tuberculous  pneumonia, 
on  the  contrary,  may  develop  with  equal  rapidity,  but  usually  remains 
stationary. 


1  Fortschr.  a.  d.  Gebiete  d.  Rontgenstrahlen.     Erganzungsband,  190S,  vol.  xix. 


204  DISEASES  OF  THE  LUNGS 

Blood. — The  presence  of  protective  substances  in  the  blood  has 
been  discussed  under  Immunity.  Invasion  of  the  blood  by  pneumo- 
cocci  is  considered  under  Pneumococcus  Septicemia.  The  oxygen 
and  carbon-dioxide  content  of  the  blood  is  given  in  the  section  on 
Metabolism.    Other  features  are  considered  under  this  heading. 

During  the  course  of  pneumonia,  the  hemoglobin  and  red  cells  are 
practically  normal.  After  defervescence  the  hemoglobin  and  red  cells 
are  usually  below  normal.  The  hemoglobin  falls  proportionally  lower 
than  the  red  cells  and  the  blood  picture  is  that  of  a  mild  secondary 
anemia.  During  convalescence  the  number  of  red  cells  may  fall  for 
a  week  to  ten  days  and  then  gradually  return  to  normal. 

White  Cells.— In  Cabot's1  series  of  842  cases,  the  leukocyte  count 
at  the  time  of  entrance  to  the  Massachusetts  General  Hospital  was 
as  follows : 

Under         10,000  =  90  (83  fatal) 

Between    10,000  to  15,000—125 

15,000  to  20,000—192 

20,000  to  25,000—186 

25,000  to  30,000—114 

30,000  to  35,000—  47 

35,000  to  40,000—  44 

40,000  to  45,000—  20 

45,000  to  50,000—  10 

50,000  to  55,000—     7 

55.000  to  60,000—     2 

60,000  to  65,000—     3 

65,000  to  70,000—     1 

100,000  to  110,000—     1 

Of  500  cases  in  the  present  series,  also  from  the  Massachusetts 
General  Hospital,  the  following  counts  were  obtained  at  the  time  of 
entering  the  hospital : 

White  cells.  No.  of  cases. 

1  to  5,000 10 

5  to  10,000 35 

10  to  15,000 86 

15  to  20,000 99 

20  to  25,000 103 

25  to  30,000 67 

30  to  35,000 49 

35  to  40,000 14 

40  to  45,000 15 

45  to  50,000 12 

50  to  55,000 2 

55  to  60,000 3 

60  to  65,000 1 

65  to  70,000 1 

70  to  75,000 1 

75  to  80,000 1 

100,000 1 

A  leukocytosis  (above  10,000)  was  observed  in  455  (90  per  cent.) 
of  the  500  cases.  In  more  than  one-half,  the  count  was  from  15,000 
to  30,000.    The  leukocytosis  was  somewhat  more  marked  in  children 

1  Clinical  Examination  of  the  Blood,  1904. 


LOBAR  PNEUMONIA  205 

than  in  adults,  and  the  only  instance  in  the  series  in  which  the  count 
reached  100,000  was  in  a  child  of  two  years  and  ten  months.  In  this 
series,  no  constant  relation  appears  to  obtain  between  the  degrees  of 
leukocytosis  and  the  severity  of  the  infection,  but  it  is  to  be  noted  that 
the  mortality  was  relatively  high  among  those  without  leukocytosis. 
Thus,  of  the  45  cases  with  counts  below  10,000,  22  (48.8  per  cent.) 
died.  Of  90  cases  in  Cabot's  series  without  leukocytosis,  83  (92.2 
per  cent.)  died. 

An  increase  in  the  leukocytes  usually  occurs  as  early  as  the  time  of 
the  chill  or  a  few  hours  after  it,  and  continues  throughout  the  disease. 
The  counts,  whether  high  or  low,  are  likely  to  be  maintained  at  a  nearly 
constant  level  without  relation  to  the  temperature,  throughout  the 
height  of  the  disease,  but  in  exceptional  instances  a  low  or  high  count 
shows  a  tendency  to  rise  or  fall.  The  leukocytes  do  not  fall  with  the 
drop  in  the  temperature,  but  their  number  slowly  diminishes  and  in 
favorable  cases  may  reach  normal  within  a  week  to  ten  days  after 
defervescence.  In  delayed  resolution  and  in  the  presence  of  compli- 
cations due  to  suppuration,  the  leukocytosis  usually  persists  until 
the  lung  clears  or  the  complication  is  relieved. 

Differential  Counts. — During  the  febrile  period  the  poly  nuclear 
neutrophiles  usually  comprise  from  80  to  90  per  cent,  or  more  of  the 
white  cells  and  a  relative  increase  in  their  number  may  be  observed 
even  in  cases  without  leukocytosis.  Their  proportion  diminishes  with 
the  crisis  and  during  convalescence,  and  a  relative  lymphocytosis 
may  be  present  after  the  white  count  has  reached  normal.  Eosino- 
phils are  diminished  or  absent  during  the  febrile  period.  According 
to  Cabot,  the  eosinophils  and  blood  plates  are  above  normal  after 
the  crisis  and  the  eosinophiles  may  run  up  to  5  or  6  per  cent. 

Iodophilia. — According  to  Cabot,1  this  is  present  and  marked  in 
practically  all  cases.  Dunn  (quoted  from  Cabot)  has  noted  that  while 
in  cases  ending  in  crisis  and  resolution  the  reaction  disappears  in  a  day 
or  two,  it  persists  in  those  with  delayed  resolution. 

Coagulation  Time. — An  increase  in  the  rapidity  of  coagulation  has 
long  been  thought  to  occur  during  pneumonia.  Cohen2  found  the 
average  time  for  coagulation  slightly  shortened  in  6  cases.  Hayem3 
Pye-Smith,4  Coleman,5  and  Dochez6  found  it  prolonged. 

Complications. — Bronchitis. — The  history  of  an  acute  infection  of 
the  upper  parts  of  the  respiratory  tract  may  be  obtained  in  a  consider- 
able proportion  of  patients  with  pneumonia,  and  it  is  probable  that 
a  bronchitis  due  to  the  pneumococcus  may  be  the  starting  point  of  the 
disease.  Bronchitis  involving  the  terminations  of  the  bronchi  in  the 
affected  region  is  constant  during  the  course  of  the  infection  and  diffuse 
bronchial  involvement  is  often  noted.  Laryngitis  is  rare.  Edema 
of  the  larynx  and   suppurative  perichondritis  have  been  reported. 

1  Loc.  cit.,  p.  193.  -  Arch.  Int.  Med.,  1911,  viii,  684,  820. 

3  Du  Sang.,  etc.,  Paris,  1889,  p.  323.  4  Allbutt's  System  of  Med.,  1S98,  v,  91. 

6  Biochem.  Jour.,  1907,  ii,  184.  6  Jour.  Exp.  Med.,  1912,  vol.  xvi. 


206  DISEASES  OF  THE  LUNGS 

Pleuritis,  Serofibrinous  and  Purulent  Effusions. — Fibrinous  inflammation 
of  the  pleura  over  the  involved  part  of  the  lung  or  a  wider  area  is 

almost  constant  in  lobar  pneumonia.  A  varying  but  usually  small 
amount  of  fluid  was  present  in  57  (37  per  cent.)  of  1  54  autopsies  at  the 
Massachusetts  General  Hospital.  Small  effusions  are  usually  sero- 
fibrinous. Of  the  57  cases  the  fluid  was  clear  or  cloudy  in  40,  purulent 
in  9  and  hemorrhagic  in  6.  Microscopic  examination  after  sedimenta- 
tion shows  varying  proportions  of  polynuclear  leukocytes,  lymphocytes, 
large  mononuclear  and  endothelial  cells.  Even  in  clear  fluids  with 
low  percentages  of  polynuclear  cells,  cultures  may  demonstrate  pneu- 
mococci  or  other  organisms.  The  pneumococci  may  be  of  diminished 
virulence.  Empyema  was  present  in  2.2  per  cent,  of  13,550  cases  of 
pneumonia  collected  by  Musser  and  Xorris  and  in  19  (3.8  per  cent.) 
of  500  cases  at  the  Massachusetts  General  Hospital.  A  serofibrinous 
effusion  complicated  the  pneumonia  in  5  (1.0  per  cent.)  of  the  cases. 
The  greater  frequency  of  an  effusion  among  autopsied  cases  must  be 
ascribed  to  the  readiness  with  which  a  small  collection  is  overlooked 
during  life.  The  subject  is  further  considered  in  the  section  on 
Pleuritis. 

Pneumothorax. — This  ma}-  follow  the  perforation  of  empyema  into  the 
lung  or  the  rupture  of  an  area  of  pulmonary  abscess  or  gangrene  into 
the  pleura.  Lobar  pneumonia  is  to  be  regarded  as  a  cause  only  in  so 
far  as  it  leads  to  conditions  to  which  the  pneumothorax  may  be 
secondary. 

Abscess  and  Gangrene. — So  far  as  they  relate  to  lobar  pneumonia, 
abscess  and  gangrene  are  of  rare  occurrence,  occurring  in  only  76 
(0.G3  per  cent.)  of  12,030  cases  collected  by  Musser  and  Xorris,  in 
scarcely  2  per  cent,  of  Frankel's,1  and  in  only  2  (0.4  per  cent.)  of 
500  cases  in  this  series.  They  are  more  common  among  autopsied 
cases,  suggesting  that  they  not  infrequently  escape  detection  clini- 
cally, and  that  small  losses  of  pulmonary  substance  spontaneously 
heal.  A  more  detailed  discussion  of  this  subject  will  be  found  in  the 
chapter  on  Abscess  and  Gangrene. 

Mediastinitis. — Weichselbaum2  noted  acute  inflammatory  edema 
of  the  areolar  tissue  in  the  mediastinum,  the  neck,  clavicular  fossae 
and  about  the  trachea,  esophagus  and  cervical  vertebra?,  and  his 
findings  were  confirmed  by  Foa  and  Bordoni-Uffreduzzi.3  Time4 
followed  the  pneumococcus  infection  through  the  lymph  vessels  of 
the  pulmonary  pleura  to  the  mediastinum  and  the  pericardium. 
Frankel  observed  purulent  mediastinitis  as  a  complication  of  fibrinous 
pneumonia  in  3  cases.  An  abscess  may  perforate  the  chest  wall  beside 
the  sternum  as  in  one  of  Frankel's  cases.  In  a  second  of  his  cases, 
dulness  over  an  area  4  cm.  wide  was  present  near  the  right  border  of  the 

'  Deut.  med.  Woch.,  Vercins  Beilage,  1903,  p.  204. 

2  Wiener  med.  Jahrbucher,  1886,  N.  F.,  p.  532. 

3  Zeit.  f.  Hyg.,  Bd.  iv,  p.  75. 

*  Zentralb.  f.  Bakteriol.  u.  Parasitenk,  1889,  Bd.  v,  p,  38. 


LOBAR  PNEUMONIA  207 

sternum  between  the  clavicle  and  the  fourth  rib,  with  systolic  pulsa- 
tion in  the  second  intercostal  space.  The  diagnosis  is  difficult,  and 
diffuse  infiltration  may  give  no  indication  of  its  presence,  but  abscess 
formation  may  be  detected  by  the  presence  of  dulness  with  diminished 
breathing  in  .the  supracardiac  region  or  over  the  spine  between  the 
third  and  the  ninth  dorsal  vertebrae.  X-ray  examination  may  be  of 
assistance  in  diagnosis.  Complicating  pericarditis,  peritonitis,  and 
empyema  may  also  be  present.  An  abscess  may  rupture  into  the 
bronchus  with  recovery. 

Subphrenic  Abscess.— Pneumonia  is  only  rarely  a  cause.  Cases  have 
been  reported  by  Lampe,1  Claudius,2  Winkelmann,3  and  others.  The 
literature  of  subphrenic  abscess  is  reviewed  by  Perutz.4 

Cardiovascular  System. — Myocardial  weakness  of  varying  degree  is 
an  important  feature  in  pneumonia.  It  is  due  to  obstruction  of  the 
pulmonary  circuit  and  to  toxemia,  and  is  more  marked  in  cases  with 
preexisting  myocardial,  endocardial  or  pericardial  disease,  or  in  those 
with  arteriosclerosis  or  chronic  renal  changes.  In  most  cases,  however, 
recovery  from  pneumonia  is  not  followed  by  lasting  cardiovascular 
disturbance  which  can  be  ascribed  to  the  infection. 

Endocarditis. — Bouillard5  first  pointed  out  that  pneumonia  was  one 
of  the  causes  of  endocarditis,  and  Herschl6  reported  5  cases  of  ulcera- 
tive endocarditis  following  pneumonia  and  complicated  by  meningitis. 
In  1886,  Netter7  analyzed  73  cases  from  the  literature  and  added  nine 
personal  observations,  seven  with  bacteriologic  examination  of  the 
lesions.  Preble8  found  50  cases  added  to  the  literature  since  that  time 
and  reviewed  the  entire  132  cases.  The  frequency  with  which  pneu- 
monia is  a  cause  is  shown  by  Wells'9  analysis  of  517  fatal  cases  of 
endocarditis,  of  which  115  (22.2  per  cent.)  were  in  connection  with 
pneumonia. 

Acute  endocarditis  is  fortunately  not  a  common  complication  of 
pneumonia,  however,  being  noted  in  only  144  (0.44  per  cent.)  of 
Musser  and  Norris'  32,349  collected  cases.  Frankel  observed  endo- 
carditis in  pneumonia  clinically  in  only  0.8  per  cent,  of  his  cases; 
Aufrecht10  only  once  among  1500  cases.  It  was  detected  during  life 
in  none  of  500  cases  at  the  Massachusetts  General  Hospital,  but  was 
found  in  7  (4.5  per  cent.)  of  154  cases  at  autopsy.  In  autopsy  cases 
collected  by  Preble,  86  (4.28  per  cent.)  instances  of  endocarditis  were 

1  Munch,  med.  Woch.,  14  Mai,  1895. 

2  Hospitalstidende,  1898,  Bd.  vi;   see  Jahrb.  v.  Virchow-Hirsch,  Bd.  ii,  p.  381. 

3  Deut.  med.  Woch.,  1899,  No.  7. 

*  Centralb.  f.  d.  Grenzgeb.  d.  Med.  u.  Chir.,  1905,  8. 

5  Traite  clinique  des  malad.  du  coeur.,  1862. 

6  Osterr.  Zeit.  f.  prakt.  Heilk.,  1862. 

7  De  l'endocardite  vegetante  ulcereuse  d'origine  pneumonique,  Arch,  de  Physiol, 
norm,  et  path.,  1886,  p.  10. 

s  Amer.  Jour.  Med.  Sci.,  1904,  N.  S.,  cxxviii,  782. 
9  Jour.  Amer.  Med.  Assoc,  1902,  xxxix,  978. 

10  Nothnagel's  Encyclopedia  of  Pract.  Med.,  American  edition.Diseases  of  the  Bronchi, 
Pleura,  and  Lungs,  p.  490. 


208  DISEASES  OF  THE  LUNGS 

present  in  1775  cases.  Preble  places  the  average  at  about  1  per  cent. 
of  all  cases  and  5  per  cent,  of  the  fatal  cases.  The  discrepancy  between 
clinical  and  autopsy  cases  indicates  that  it  must  be  frequently  over- 
looked. Xot  all  cases  of  acute  endocarditis  developing  in  the  course 
of  pneumonia  are  due  to  the  pneumococcus.  Preble  estimates  that 
something  over  94  per  cent,  are  due  to  this  organism. 

The  endocarditis  due  to  infection  with  pneumococci  does  not  appear 
to  differ  from  that  caused  by  other  organisms.  In  its  early  stages  there 
are  small,  reddish,  Mesh-like  vegetations,  usually  at  the  margins  of  the 
valves.  These  may  later  assume  a  polypous  or  ulcerative  type,  and 
Preble  estimates  that  the  chances  are  four  to  one  that  an  endocarditis 
developing  in  the  course  of  pneumonia  will  be  of  the  so-called  ulcerative 
or  malignant  type.  The  process  may  not  be  confined  to  the  valves, 
but  may  involve  the  endocardium  as  well.  In  cases  in  which  recovery 
from  the  acute  infection  follows,  chronic  fibrous  endocarditis  develops. 
Valves  already  the  site  of  chronic  inflammatory  changes  may  become 
acutely  inflamed  during  the  course  of  pneumonia.  Of  50  cases  in 
Preble's  series,  12  showed  old  endocarditis  upon  which  fresh  vegeta- 
tions had  developed.  Among  the  154  autopsied  cases  in  the  Massa- 
chusetts General  Hospital  series  were  29  with  chronic  endocarditis, 
one  of  which  was  complicated  by  an  acute  endocarditis.  The  left 
side  of  the  heart  is  affected  in  a  large  proportion  of  the  cases,  in  82 
per  cent,  of  Preble's  series,  while  the  right  side  was  involved  in  12  per 
cent,  and  both  sides  in  5.7  per  cent.  In  his  series  the  aortic  valve  was 
alone  involved  in  39.7  per  cent,  the  mitral  alone  in  28.3  per  cent., 
both  aortic  and  mitral  in  14.1  per  cent.,  the  tricuspid  alone  in  8.5  per 
cent.,  the  pulmonary  alone  in  3.6  per  cent.,  aortic,  mitral,  and  tricuspid 
in  3.5  per  cent.,  the  mitral  and  tricuspid  in  1.4  per  cent.,  and  the 
aortic  and  tricuspid  in  0.7  per  cent.  Infarcts  occurred  in  about  one- 
half  the  cases.  Meningitis  complicated  the  pneumococcus  endocar- 
ditis in  about  60  per  cent,  of  the  cases.  The  complication  is  much  more 
frequent  after  thirty  years  of  age  than  before. 

The  clinical  features  are  those  writh  other  forms  of  acute  endocar- 
ditis. The  initial  symptoms  are  usually  masked  by  those  due  to  the 
pneumonia.  Systolic  murmurs  are  so  frequently  heard  during  pneu- 
monia that  they  have  little  diagnostic  value  unless  they  vary  from  the 
functional  type.  Diastolic  murmurs  are  of  more  importance  and 
may  be  regarded  as  due  to  acute  endocarditis  when  they  develop 
under  observation  during  an  attack  of  pneumonia.  A  continuance 
of  fever  after  the  period  of  its  expected  decline  or  its  reappearance 
after  an  afebrile  period,  recurring  chills  and  sweats,  persistent  leuko- 
cytosis, ephemeral  areas  of  nodular  erythema  or  purpura,  and  the 
finding  of  pneumococci  in  blood-cultures  are  important  signs.  In  the 
cases  in  which  the  endocarditis  develops  during  the  pneumonia  and 
runs  a  rapidly  fatal  course,  the  diagnosis  is  usually  impossible. 

The  prognosis  is  grave.  Of  132  cases  in  Preble's  series  only  4 
recovered,  and  in  but  one  of  these  was  the  diagnosis  complete.    But 


LOBAR  PNEUMONIA  209 

the  frequency  with  which  patients  with  chronic  endocarditis  give  a 
history  of  acute  pneumonia  as  the  probable  starting  point  of  the  endo- 
cardial infection  makes  the  outlook  somewhat  more  hopeful  than  these 
figures  seem  to  indicate. 

Pericarditis. — Acute  pericarditis  of  the  serous,  plastic  or  purulent 
variety  was  found  in  499  (1.2  per  cent.)  among  40,773  collected  cases 
by  Musser  and  Norris  and  in  268  (12.6  per  cent.)  of  2128  autopsied 
cases.  The  proximity  of  the  pericardium  to  the  pleura  and  the  lung  is 
responsible  for  the  frequency  with  which  pericarditis  occurs  in  pneu- 
monia. Infection  by  extension  is  probably  the  most  common  method 
of  origin,  but  may  also  occur  through  the  blood  or  lymph  stream.  A 
variable  and  usually  small  amount  of  serous  fluid  was  found  in  the 
pericardial  sac  in  28  of  154  autopsied  cases  at  the  Massachusetts 
General  Hospital.  In  many  of  these  the  fluid  was  doubtless  due  to 
cardiac  insufficiency;  in  others  the  presence  of  a  small  amount  of  fibrin 
indicated  an  inflammatory  origin.  In  16  other  cases  there  was  a  fibrin- 
ous or  purulent  exudate.  These  cases  suggest  that  pericarditis  is 
more  frequent  when  the  left  lung  is  the  site  of  the  pneumonia.  In  the 
16  cases  the  left  lung  was  involved  in  12,  the  left  lung  being  involved 
alone  in  6,  both  left  and  right  lung  in  6. 

As  pericarditis  usually  complicates  the  pneumonia  at  the  height 
of  the  disease,  pain  referable  to  the  pericardium  may  be  lacking  or 
masked  by  that  due  to  pleurisy.  The  condition  is  frequently  over- 
looked during  life  and  first  found  at  postmortem  examination.  Daily 
examination  of  the  heart  should  be  made  in  all  cases  of  pneumonia. 
Pericardial  friction  may  be  heard  or  obscured  by  loud  bronchial  rales, 
pleural  friction  or  stertorous  breathing.  If  inaudible  it  may  be  pal- 
pated. A  careful  note  concerning  the  upper  and  lateral  percussion 
limits  of  the  heart,  the  intensity  and  position  of  the  cardiac  impulse 
and  the  strength  of  the  cardiac  sounds  should  be  made  at  the  first 
visit  in  all  cases  of  pneumonia,  in  order  that  any  subsequent  changes 
may  be  quickly  noted  and  an  effusion  detected  early.  Pain  on  pressure 
over  the  lower  sternal  region  may  be  present.  Dyspnea  out  of  pro- 
portion to  that  which  can  be  accounted  for  by  other  features  is  sug- 
gestive. Dysphagia,  paradoxical  pulse,  distention  of  the  veins  of  the 
neck  and  aphonia  may  be  present.  Diminution  or  disappearance  of 
the  cardiac  impulse;  enlargement  of  the  percussion  limits,  especially 
upward  and  to  the  left,  downward  and  to  the  right,  with  the  forma- 
tion of  an  obtuse  cardiohepatic  angle,  and  downward  and  to  the  left 
so  that  the  percussion  limit  in  this  region  extends  beyond  the  palpable 
impulse  of  the  heart;  disappearance  or  diminution  of  the  pericardial 
friction,  and  weakening  of  the  heart  sound  are  of  most  significance. 
X-ray  examination  is  of  assistance  in  the  diagnosis  of  doubtful 
cases. 

Pericarditis  adds  to  the  gravity  of  the  pneumonia  by  mechanically 
embarrassing  the  heart,  weakening  the  heart  muscle  in  consequence 
of  the  associated  myocarditis  and  adding  to  the  area  of  the  infected 
14 


210  DISEASES  OF  THE  LUNGS 

territory.  Of  207  cases  in  Musser  and  Norris'  scries,  125  (60  per 
cent.)  died. 

Vascular  Lesidns. — Peripheral  venous  thrombosis  is  an  uncommon 
complication.  It  was  noted  in  10  (1  per  cent.)  of  94!)  cases  by  Sears 
and  Larrabee*  and  in  3  of  500  cases  by  Steiner,2  who  lias  reviewed 
38  previously  reported.  In  27  of  32  cases  the  thrombosis  occurred 
during  convalescence,  in  one  on  the  day  of  crisis  and  in  4  during  the 
course  of  the  disease.  It  is  to  be  regarded  in  general  rather  as  a 
sequel  than  a  complication.  The  lower  extremities  were  always 
involved,  and  the  left  extremity  more  often  than  the  right.  Of  the 
41  cases,  9  died,  25  recovered  and  no  definite  information  was  given 
in  7.  Postmortem  examination  in  8  of  the  fatal  cases  showed  that 
death  was  due  to  pulmonary  embolism  in  5. 

Arterial  embolism  occurs,  but  is  still  less  common.  Embolism  of 
the  popliteal  artery  following  pneumonia  is  reported  by  Irish.3  Gibson4 
had  3  cases  of  gangrene  of  the  leg  developing  suddenly  in  the  course 
of  pneumonia.  In  Aldrich's5  case  there  was  embolism  of  one  of  the 
lenticulo-optic  arteries.  The  emboli  may  come  from  thrombi  in  the 
pulmonary  veins  of  the  pneumonic  lung  or  cardiac  thrombi. 

Gastro-intestinal  System. — Pneumococcus  gastritis  and  membranous 
colitis  have  been  observed.  Acute  dilatation  of  the  stomach  is  a  rare 
complication.  Fussell6  collected  6  cases  from  the  literature  and  added 
5  of  his  own.  Of  the  11  cases,  6  died  and  5  recovered.  Dilatation 
occurred  before  the  crisis  in  8,  after  the  crisis  in  3.  Vomiting,  abdominal 
pain,  distention,  constipation,  collapse,  splashing  sounds  and  visible 
gastric  peristalsis  should  suggest  the  diagnosis. 

Peritonitis. — This  is  rare.  It  was  found  clinically  in  28  (0.34  per 
cent.)  of  8132  cases  and  at  autopsy  in  21  (2.16  per  cent.)  of  971  cases  by 
Musser  and  Norris.  Acute  purulent  peritonitis  was  found  in  5  (3.2  per 
cent.)  of  154  cases  at  autopsy  in  the  Massachusetts  General  Hospital 
series.  General  pneumococcus  peritonitis  secondary  to  pneumonia 
is  practically  always  fatal.  Circumscribed  peritonitis  is  occasionally 
observed  and  recovery  may  follow  operation.  It  is  to  be  remembered 
that  abdominal  pain,  spasm  and  tenderness  are  not  infrequent  in 
pneumonia,  in  consequence  of  irritation  of  the  terminal  branches 
of  the  lower  intercostal  nerves.  The  possibility  of  pneumonia  should 
be  excluded  in  all  acute  abdominal  conditions. 

Jaundice. — Varying  degrees  of  jaundice  are  present  in  a  consider- 
able proportion  of  cases  of  pneumonia.  Owing  to  the  readiness  with 
which  slight  jaundice  may  be  overlooked  and  the  varying  estimate 
of  different  observers  as  to  what  degree  of  discoloration  is  necessary 
to  justify  the  use  of  this  term,  statistics  as  to  its  frequency  are  unreli- 

1  St.  Paul  Med.  Jour.,  1902,  iv,  451. 

2  Johns  Hopkins  Hosp.  Bull.,  June,  1902,  135. 

3  Albany  Med.  Annals,  1902,  xxiii,  205. 

4  Annals  of  Surgery,  1903,  xxxviii,  380. 
'-  Med.  News,  July  27,  1901. 

6  Aroer.  Jour,  Med.  Sci.,  1911,  cxlii,  794. 


LOBAR  PNEUMONIA  211 

able.  Blumberg1  found  jaundice  in  21  (7  per  cent.)  of  300  cases.  The 
stools  are  completely  acholic  in  only  a  part  of  the  cases.  The  cause 
of  jaundice  in  pneumonia  is  uncertain.  Banti2  holds  the  view  that  it 
is  due  to  hemolytic  action  of  the  pneumococcus.  Hemoglobinuria  was 
produced  in  rabbits  inoculated  with  pneumococci  from  cases  with 
jaundice,  but  did  not  occur  in  animals  infected  with  organisms  obtained 
from  patients  with  pneumonia  without  jaundice.  McPhedran3 
estimated  the  fragility  of  the  red  cells  in  14  cases  with  and  without 
jaundice  and  found  increased  resistance  in  the  jaundiced  cases.  The 
hemolytic  theory  needs  further  support  before  it  can  be  accepted. 
Passive  congestion  of  the  liver  from  cardiac  weakness  is  a  possible 
explanation,  but  has  little  in  its  favor  from  analogy  with  other  acute 
infectious  diseases,  and  evidence  of  a  sufficient  degree  of  venous  stasis 
to  account  for  the  symptom  is  usually  lacking.  An  increased  produc- 
tion of  bile  in  consequence  of  the  infection  is  purely  hypothetical. 
An  infective  cholangitis  is  perhaps  the  most  plausible  explanation. 
Anders4  reports  3  cases  with  cholecystitis  as  a  complication  of  pneu- 
monia. Jaundice  was  present  in  two  and  pyriform  enlargement  of  the 
gall-bladder  in  the  3  cases.  Clairmont5  has  reported  cholangitis  and 
abscess  about  the  gall-bladder  in  a  woman,  aged  seventy-nine  years, 
with  pneumonia  due  to  Friedlander's  pneumobacillus.  Gilbert  and 
Grenet6  found  the  colon  bacillus  in  the  bile  in  3  cases  of  pneumonia 
complicated  by  jaundice. 

The  mortality  in  some  series  of  cases  with  jaundice  is  higher  than 
in  those  not  so  complicated.  In  Mosler's7  15  cases  it  was  73  per  cent., 
and  in  Norris'8  61  per  cent.  In  other  series  there  is  little  or  no  differ- 
ence in  the  mortality  among  those  with  and  those  without  jaundice. 
Whether  the  jaundice  itself  influences  the  mortality  is  uncertain. 

Acute  Parotitis. — This  is  a  rare  complication.  Jurgensen9  found 
six  instances  among  5738  cases  of  pneumonia.  Norris10  found  one  in 
500  cases  at  the  Pennsylvania  Hospital  and  collected  17  from  the  liter- 
ature. It  may  occur  during  the  course  of  the  disease,  at  the  time  of 
defervescence  or  in  convalescence.  In  Fischel's11  case  it  did  not  develop 
until  twenty  days  after  the  crisis.  One  gland  only  is  usually  affected. 
In  a  small  proportion  both  are  involved.  Infection  may  take  place 
through  the  blood  and  give  rise  to  the  so-called  metastatic  parotitis, 
but  direct  extension  from  the  mouth  by  way  of  Stenson's  duct  is  prob- 
ably more  common,  as  is  suggested  by  the  more  frequent  presence  of 

1  St.  Petersburg  med.  Woch.,  1907,  No.  21,  p.  203. 

2  Centralb.  f.  Bak.,  1896,  xx,  849. 

3  Johns  Hopkins  Hosp.  Bull.,  1911,  xxii,  408. 

4  Amer.  Med.,  March  18,  1905,  p.  431. 
6  Wien.  klin.  Woch.,  October  26,  1S99. 

6  Arch.  gen.  de  med.,  February,  1899. 

7  Deut.  Arch.  f.  klin.  Med.,  1872,  x,  266. 

8  Osier  and  McCrae's  Mod.  Med.,  vol.  ii,  p.  613. 

9  Handb.  d.  spec.  Path.  u.  Ther.,  v.  Ziernssen,  5,  ii,  122. 

10  Philadelphia  Med.  Jour.,  April  27,  1901. 

11  Prag.  med.  Woch.,  1893,  xviii,  69. 


212  DISEASES  OF  THE  LUNGS 

other  organisms  than  the  pneumococcus  in  the  pus  from  the  gland  in 
the  few  instances  in  which  cultures  have  been  made.  The  affected 
gland  is  painful,  swollen  and  hard.  The  swelling  may  subside  sponta- 
neously or  suppuration  may  follow.  In  DuplayV  case,  pus  could  be 
expressed  from  Stenson's  duct.  Spontaneous  evacuation  of  pus  into 
the  mouth  through  Stenson's  duct  and  recovery  after  the  discharge 
had  lasted  more  than  six  weeks  is  reported  by  Pichler.2 

Nephritis. — A  mild  degree  of  renal  irritation  is  common  in  pneu- 
monia, as  indicated  by  the  presence  of  varying  amounts  of  albumin 
and  tube  casts,  but  the  urine  almost  invariably  returns  to  normal  after 
the  acute  infection  subsides.  Outspoken  nephritis  occurs  only  in  rare 
instances,  and  was  noted  by  Frankel3  among  750  cases  in  only  6 
(0.8  per  cent.),  with  4  deaths.  In  the  4  fatal  cases,  the  unfavorable 
outcome  was  rather  to  be  ascribed  to  the  pneumonia  than  to  the 
nephritis.  In  the  2  remaining  cases  the  renal  symptoms  lasted  for 
one  and  one-half  and  four  months.  Cardiac  hypertrophy  was  not 
observed  and  the  albumin  and  formed  elements  disappeared  from  the 
urine.  Of  500  cases  at  the  Massachusetts  General  Hospital,  acute 
nephritis  with  edema  developed  in  only  one  (761-229),  and  wras  followed 
by  recovery.  In  fatal  cases  cloudy  swelling  and  fatty  degeneration 
of  the  renal  epithelium  is  common.  Pneumococci  may  be  found  in  the 
kidney,  as  in  22  of  26  cases  examined  by  Frankel  and  Reiche,4  but 
evidence  of  sufficiently  intense  renal  changes  to  justify  the  term  acute 
nephritis  is  found  only  in  uncommon  instances.  In  such  cases  the 
action  of  the  toxin  is  for  the  most  part  upon  the  glomeruli.  In  2 
of  154  cases  at  autopsy,  an  acute  intracapillary  glomerulonephritis 
was  found.  Acute  nephritis  rarely  terminates  in  the  chronic  form. 
The  history  of  pneumonia  as  the  starting  point  of  chronic  nephritis 
is  seldom  obtained.  Eisenlohr5  has  reported  the  finding  at  autopsy 
of  outspoken  contracted  kidney  ten  months  after  the  onset  of  acute 
nephritis  with  pneumonia. 

Nervous  System. — Symptoms  indistinguishable  from  those  with 
meningitis  and  probably  toxic  in  origin  may  be  present,  and  menin- 
gitis may  be  absent  at  autopsy.  These  cases  have  been  spoken  of 
under  Meningismus  in  a  previous  section.  Otitis  media  should  be 
suspected  in  children  with  marked  cerebral  symptoms. 

Meningo-encephalitis.  —  Weichselbaum6  described  acute  meningo- 
encephalitis due  to  the  pneumococcus.  Three  cases,  classed  in  this 
category,  have  been  reported  by  Kirchheim,7  who  finds  similar  observa- 
tions by  Dornberger,8Hensinger,9  v.  Lengerke,10Hereus,u  and  Schultze.12 

1  La  Semainc  med.,  1891,  xi,  9.  2  Wiener  klin.  Woch.,  1903,  No.  49,  p.  1361. 

3  Loc.  cit.,  p.  360.  "  Zeit.  f.  klin.  Med.,  Bd.  xxv,  p.  278. 

s  Deut.  med.  W^och.,  1892,  No.  32,  p.  732. 

6  Wiener  klin.  Woch.,  1888,  No.  28.      7  Med.  Klinik,  1908,  Nr.  38,  p.  1461. 

8  Munch,  med.  Woch.,  1904,  Nr.  19. 

s  Deut.  med.  Woch.,  1886,  Nr.  12,  p.  37. 
io  Mitt.  a.  d.  Tubinger  Poliklinik,  Leipzig,  1882,  H.  2. 
»  Ibid.,  1892,  H.  2. 
12  Nothnagel's  Handb.,  Bd.  ii,  Verhandl.  d.  6  Kong.  f.  inn.  Med. 


LOBAR  PNEUMONIA  213 

In  the  course  of  or  after  pneumonia,  symptoms  of  localized  cerebral 
involvement  are  observed,  such  as  disturbances  of  the  cranial  nerves, 
monoplegia,  convulsive  movements  of  one  or  more  of  the  extremities, 
ataxia,  etc.  The  pathology  is  not  clear,  but  meningo-encephalitis  is  sug- 
gested by  Kirchheim.    The  outlook  for  complete  recovery  is  uncertain. 

Meningitis. — This  occurred  in  206  (0.42  per  cent.)  among  49,028 
clinical  cases  collected  by  Musser  and  Norris  and  in  180  (3.5  per  cent.) 
of  4833  autopsied  cases.  It  was  present  in  only  2  (0.4  per  cent.)  of 
500  clinical  cases  and  in  4  (2.5  per  cent.)  of  154  cases  at  autopsy  in 
this  series.  Liebermeister1  found  meningitis  on  microscopic  examination 
in  3  of  11  cases  of  pneumonia  at  autopsy.  In  these  cases  macroscopic 
examination  showed  no  evidence  of  meningitis  (!).  The  complication 
usually  occurs  while  the  disease  is  at  its  height.  Infection  may  take 
place  by  extension  from  the  ethmoid  cells,  the  antrum  of  Highmore, 
the  sphenoidal  sinus,  the  middle  ear  or  mastoid.  It  is  possible  that 
infection  of  the  nasal  sinuses  may  arise  by  extension  through  the  areolar 
tissue  of  the  neck  from  the  mediastinum.  In  some  cases  no  local 
source  can  be  found,  and  in  such  instances  the  meninges  may  be 
invaded  through  the  blood,  but  the  almost  constant  presence  of  pneu- 
mococci  in  the  blood  and  the  rarity  of  meningitis  suggests  that  some- 
thing more  than  bacteriemia  must  be  responsible.  The  pathologic 
picture  in  pneumococcus  meningitis  does  not  differ  from  that  due  to 
the  meningococcus  or  the  influenza  bacillus.  The  exudate  is  purulent 
and  of  variable  distribution,  but  usually  involves  the  entire  cerebro- 
spinal system.  The  symptoms  are  often  masked  by  stupor  and  delirium 
so  common  in  severe  forms  of  the  disease.  Headache,  nausea  and 
vomiting,  delirium,  stiffness  of  the  neck  and  retraction  of  the  head 
are  suggestive,  but  may  be  present  without  meningitis.  Opisthotonos 
and  epileptiform  convulsions  may  be  observed.  Paralysis  of  cranial 
nerves,  monoplegia,  hemiplegia,  optic  neuritis,  Brudzinski's  or  Kernig's 
sign  are  more  definite  indications.  The  diagnosis  may  be  established 
by  lumbar  puncture. 

Meningitic  symptoms  may  occasionally  initiate  the  attack,  and 
evidence  of  pneumonia  appear  later.  In  rare  instances,  meningitis 
may  occur  some  time  after  the  attack  of  pneumonia.  In  the  case 
reported  by  de  Chezelle  and  Prieur2  a  pneumococcus  meningitis 
occurred  three  months  after  pneumonia.  Cases  in  which  purulent 
fluid  containing  pneumococci  is  obtained  by  lumbar  puncture  have 
apparently  thus  far  always  proved  fatal.  Holt3  has  reported  the  case 
of  a  child  of  two  with  pneumonia,  twitching  of  the  hands,  fingers  and 
face,  rigidity  of  the  neck,  retraction  of  the  head  and  definite  convulsive 
movements  of  the  extremities.  Lumbar  puncture  showed  clear  fluid 
under  high  tension,  without  cells,  but  containing  pneumococci. 
Recovery  was  complete. 

1  Munch,  med.  Woch..  1909,  No.  15,  p.  750. 

2  Arch,  de  med.  et  de  pharm.  militaires,  1892,  T.  20. 
5  Arch,  of  Pediatrics,  New  York,  1906,  23. 


214  DISEASES  OF  THE  LUNGS 

Inequality  of  the  Pupils. — Inequality  of  the  pupils  with  dilatation 
on  the  affected  side  is  occasionally  observed.  Xorris1  examined  64 
patients  with  speeial  reference  to  the  condition  of  the  pupils,  and  found 
mydriasis  in  one  and  myosis  in  another  on  the  affected  side.  The 
upper  lobe  was  involved  in  33.  Dilatation  of  the  pupil  on  the  affected 
side  may  be  ascribed  to  irritation  of  the  cervical  sympathetic. 

Reflexes. — Schultze2  observed  absence  of  the  pupillary  light  reflex 
in  4  cases  during  pneumonia  and  return  of  the  reaction  later  to  normal. 
Absence  of  the  patellar  reflex  during  pneumonia  has  been  observed 
by  Marinian,3  Longard,4  and  Sternberg.5 

Tetany  in  the  course  of  pneumonia  was  observed  by  Siredey  and 
Lemaire.6 

Hemiplegia  is  rarely  a  complication.  Cerebral  hemorrhage,  throm- 
bosis or  embolism  from  thrombi  in  the  pulmonary  veins  or  the  heart 
may  be  the  cause.  In  a  case  of  bulbar  and  ascending  paralysis,  Seitz7 
found  organisms  resembling  pneumococci  in  the  central  nervous 
system. 

Neuritis. — Paralysis  of  the  ocular  muscles,  the  muscles  of  the  larynx, 
palate,  face  and  extremities  has  been  noted  to  develop  during  or  shortly 
after  pneumonia,  and  is  probably  due  to  toxic  neuritis.  Multiple 
neuritis  has  also  been  described.    The  prognosis  appears  to  be  favorable. 

Ocular  Disturbances. — These  are  not  common.  Conjunctivitis  was 
observed  in  3  of  500  cases.  In  one  case  it  was  complicated  by  an 
ulcer  of  the  cornea.  Ulcerative  keratitis  occurred  alone  in  one  case. 
Mandl3  has  reported  hypopyon-keratitis  with  sudden  establishment 
of  corneal  abscess  on  the  fourteenth  day  of  canvalescence.  The  pneu- 
mococcus  was  found  in  the  pus.  Ulcus  serpens  probably  arises  as  a 
result  of  inoculation  of  the  pneumococcus  through  a  slight  injury  of 
the  cornea.  Metastatic  panophthalmitis  has  been  described  by  Zobel,9 
Petit,10  Brown,11  and  others.  In  Wopfner's12  case,  pneumonia  and  pan- 
ophthalmia developed  five  days  after  a  cataract  operation.  Death 
occurred  five  days  later.  The  pneumobacillus  of  Friedlander  was 
found  in  the  involved  parts  of  the  lung  and  in  the  eye.  Axenfeld  and 
Goh13  observed  retinal  hemorrhages  and  small  areas  of  infiltration 
in  a  case  in  which  pneumococci  were  demonstrated  in  the  blood  before 
and  after  death.  Pneumococci  were  also  found  in  the  areas  of  retinal 
infiltration.    In  J.  Frankel's14  case,  round  white  areas  were  seen  about 

1  Osier  and  McCrae's  Mod.  Med.,  vol.  i,  p.  262. 

2  Deut.  Arch.  f.  klin.  Med.,  1902,  lxxiii,  351. 

3  Rivista  clinica,  Bologna,  1884,  p.  415. 

4  Deut.  Zeit.  f.  Nervcnheilk.,  Bd.  i,  p.  300. 

5  Die  Sehnenreflexe,  Wien  and  Leipzig,  1896. 

6  Soc.  med.  d.  Hop.  de  Paris,  1904,  T.  21,  3  S.,  p.  397. 

7  Deut.  med.  Woch.,  1897,  No.  19,  p.  290. 

8  Wiener  med.  Woch.,  1899,  No.  41.  9  Zeit.  f.  Augenh.,  vol.  xi,  p.  1. 

10  Soc.  Francaise  d'Ophtalmologie,  1901,  xviii,  426. 

11  Glasgow  Med.  Jour.,  1907,  lxvii,  484. 

12  Klin.  Monatsbl.  f.  Augenheilk,  1906,  44-1,  N.  F.,  1. 

13  Von  Graefe's  Arch.',  vol.  xliii,  p.  1.  14  Ibid.,  vol.  xlviii,  p.  456. 


LOBAR  PNEUMONIA  215 

the  macula  in  a  patient  with  pneumonia.  The  lesions  disappeared 
in  six  weeks.    Such  areas  are  probably  of  embolic  origin. 

Acute  Otitis  Media. — This  occurred  in  17  (3.4  per  cent.)  of  500  cases. 
In  9  of  these  the  patients  were  under  ten  years  of  age.  Among  42 
cases  in  which  at  autopsy  the  ears  were  examined,  otitis  media  was 
found  in  five.  The  infection  of  the  ear  may  be  the  result  of  extension 
through  the  Eustachian  tube  of  nasopharyngeal  infection  or  may  be 
hematogenous.  One  or  both  ears  may  be  affected.  The  exudate  is 
almost  invariably  purulent,  and  symptoms  simulating  meningitis 
may  be  present  before  the  drum  perforates.  Paracentesis  or  sponta- 
neous rupture  is  usually  followed  by  subsidence  of  symptoms  and 
recovery  without  loss  of  hearing.  Mastoiditis  is  occasionally  observed, 
and  in  rare  instances  extension  to  the  cerebral  sinuses  and  the  meninges. 
The  mastoid  was  involved  in  one  of  the  5  cases  with  otitis  media  at 
autopsy  in  this  series.  During  the  toxemia  of  pneumonia,  the  middle 
ears  should  be  carefully  examined  as  a  routine,  otherwise  the  compli- 
cation may  be  overlooked  and  meningitis  may  arise  by  extension,  as 
occurred  in  one  of  these  cases. 

Arthritis. — This  is  a  rare  complication.  Among  28,040  cases  col- 
lected by  Musser  and  Norris,  were  150  (0.5  per  cent.)  with  acute 
arthritis.  Of  500  cases  in  this'  series  there  were  2  with  acute  arthritis. 
Grisolle1  was  the  first  to  note  the  resemblance  between  arthritis 
in  pneumonia  and  abscess  formation  in  pyemia,  and  to  regard  the 
arthritis  complicating  pneumonia  as  distinct  from  "rheumatism." 
Weichselbaum2  was  the  first  to  demonstrate  the  pneumococcus  as 
the  cause  of  the  arthritis.  Brunner3  in  1892  collected  22  cases;  Leroux4 
in  1899  reported  28  cases.  In  1901  Cave5  brought  the  number  to  31, 
in  1902  Herrick6  made  a  total  of  52,  and  in  1903  Howard7  reported 
3  cases  and  found  the  total  number  reported  to  be  72.  The  arthritis 
may  occur  at  any  period  of  the  disease  and  attack  any  joint,  but  the 
larger  joints,  and  especially  the  knees,  seem  to  be  more  frequently 
affected.  The  infection  may  be  mono-  or  polyarticular.  Injury  to  the 
joint  from  a  sprain,  bruise  or  previous  arthritis  may  be  a  predisposing 
factor  by  diminishing  local  resistance  and  increasing  the  danger  of 
infection  by  organisms  circulating  in  the  blood.  The  process  may 
occur  as  an  arthritis,  periarthritis,  synovitis  or  bursitis,  and  in  severe 
cases  may  destroy  the  cartilage  and  even  invade  the  bone.  In  mild 
cases  there  is  local  pain,  redness,  and  swelling,  with  an  accumulation 
of  serous  fluid  and  little  general  disturbance.  In  more  severe  cases, 
in  which  the  exudate  becomes  purulent,  the  local  symptoms  are  aggra- 
vated and  the  general  disturbance  may  be  marked.  Spontaneous 
recovery  usually  occurs  in  serous  effusions,  but  a  fatal  termination  is 

1  Traite  de  la  pneumonie,  Paris,  II  ed.,  1864,  p.  384. 

2  Wiener  klin.  Woch.,  1888,  Nos.  28-32. 

3  Corresp.  f.  Schw.  Aerzte.  Jahrg.,  1892,  vol.  xxii,  Nos.  11-12. 

4  Les  Arthrites  a  Pneumocoques,  Paris,  1899. 

6  Lancet,  January  12,  1901.  6  Amer.  Jour.  Med.  Sci.,  July,  1902. 

7  Johns  Hopkins  Hosp.  Bull.,  1903,  xiv,  303. 


216  DISEASES  OF  THE  LUNGS 

common  in  the  general  infections  to  which  suppuration  in  the  joints 
is  usually  due.  An  acute  endocarditis  may  be  present.  Pneumococci 
alone  or  mixed  with  other  organisms  may  be  found  in  the  joints. 
In  some  cases  pneumococci  cannot  be  demonstrated  in  the  effusion. 
A -ray  examination  is  of  value  in  the  determination  of  the  character 
of  the  pathologic  changes. 

Diagnosis. — The  history  of  an  acute  onset  with  chill,  rapid  rise 
of  temperature,  pain  in  the  side,  cough  with  rusty  sputum  and  dyspnea, 
and  on  examination  herpes,  rapid  and  restricted  respiration  and  dulness, 
crepitant  rales,  bronchial  breathing,  increase  of  voice,  whisper  and 
tactile  fremitus  over  a  circumscribed  pulmonary  area  are  characteristic 
features.  Leukocytosis  and  the  finding  of  pneumococci  in  the  sputum 
and  the  circulating  blood  are  confirmatory.  In  typical  cases  the  diag- 
nosis is  readily  made  and  the  chief  concern  is  the  early  detection  of 
complications. 

Differential  Diagnosis. — Atypical  cases  may  present  a  difficult 
problem,  and  may  readily  be  confounded  with  acute  tuberculous 
pneumonia,  pulmonary  infarction,  bronchopneumonia,  and  pleural 
effusion.  A  variation  from  the  characteristic  picture  is  not  uncommon 
in  children  and  the  aged  and  in  those  debilitated  from  any  cause. 
Terminal  lobar  pneumonia  is  often  overlooked,  and  central  pneumonia 
may  be  in  doubt  for  several  days.  Meningitis  may  be  suspected 
when  there  are  nervous  symptoms  with  delirium  and  rigidity  of  the 
neck  and  typhoid  fever  in  cases  of  gradual  onset  without  definite 
pulmonary  signs.  Atelectasis  in  the  course  of  bronchopneumonia 
may  simulate  croupous  pneumonia  complicated  by  an  effusion.  Pas- 
sive pulmonary  congestion  with  the  expectoration  of  bloody  sputum 
and  elevation  of  temperature  from  a  complicating  bronchopneumonia 
may  also  simulate  croupous  pneumonia.  Careful  inquiry  concerning 
the  evolution  of  symptoms  and  repeated  examination  of  the  lungs  of 
patients  with  fever  of  obscure  origin  will  prevent  some  mistakes. 

In  the  consideration  of  the  various  conditions  with  which  lobar 
pneumonia  may  be  confused,  it  is  useful  to  bear  in  mind  that  consoli- 
dation of  the  lung  from  such  other  causes  as  bronchopneumonia, 
infarction  or  retraction  and  compression  of  the  lung  from  accumulation 
of  fluid  in  the  serous  sacs  gives  rise  to  similar  physical  signs,  i.  e., 
dulness,  bronchial  breathing,  increase  of  voice,  whisper,  and  tactile 
fremitus,  provided  the  bronchi  communicate  freely  with  the  consoli- 
dated area.  Pulmonary  cysts,  tumors,  atelectatic  areas  from  broncho- 
stenosis and  accumulations  of  fluid  or  solid  material  in  the  pleura  give 
rise  to  dulness  with  diminished  or  absent  breathing,  voice,  whisper,  and 
tactile  fremitus,  owing  to  the  lack  of  communication  of  the  involved 
region  with  the  bronchi.  Plugging  of  the  bronchi  in  massive  pneumonia 
gives  rise  to  signs  similar  to  those  in  the  latter  group. 

Acute  Tuberculous  Pneumonia. — This  may  present  great  difficulty 
and  a  differentiation  in  the  first  few  days  of  the  illness  may  be  im- 
possible.    There  may  be  an  abrupt  onset  with  chill,  rapid  rise  of 


LOBAR  PNEUMONIA  217 

temperature,  pain  in  the  side,  cough  and  dyspnea,  and,  on  examina- 
tion, signs  of  consolidation  as  in  croupous  pneumonia.  The  sputum 
may  even  be  rusty.  A  family  history  of  tuberculosis  or  opportunity 
for  contagion,  hemoptysis  out  of  a  clear  sky,  a  primary  pleurisy, 
adenitis  with  resultant  cervical  scars,  ischiorectal  abscess  or  other 
features  may  suggest  the  possibility  of  tuberculosis.  Cough  and 
failing  health,  evening  rise  of  temperature,  night-sweats,  and  loss  of 
weight  may  have  preceded  the  acute  onset  of  pulmonary  symptoms 
by  some  weeks  or  months.  Unusual  irregularity  in  the  temperature 
curve  and  especially  a  markedly  remittent  or  intermittent  fever, 
with  failure  of  the  temperature  to  fall  to  normal  at  the  time  of  its 
expected  decline,  absence  of  leukocytosis  during  the  febrile  period, 
apical  pneumonia,  or  signs  of  apical  disease  when  the  consolidation 
involves  the  base,  are  suggestive  features.  The  sputum  is  likely  to 
be  purulent,  and  blood  when  present  is  more  often  in  streaks  or  masses 
than  in  homogeneous  admixture.  The  sputum  is  less  tenacious  and 
viscid  than  in  croupous  pneumonia.  The  finding  of  tubercle  bacilli 
may  be  the  only  positive  indication  that  the  condition  is  not  that 
of  croupous  pneumonia,  but  when  in  selected  particles  of  sputum, 
well  washed  of  adherent  mucus  by  passage  through  several  tubes  of 
sterile  bouillon  or  salt  solution,  examination  by  means  of  smears 
and  cultures  fails  to  show  pneumococci,  tuberculosis  may  be  suspected. 
Careful  and  repeated  examination  for  tubercle  bacilli  may,  however, 
be  necessary  before  the  diagnosis  can  be  established. 

Pulmonary  Infarction. — This  may  closely  resemble  lobar  pneu- 
monia, and  the  differentiation  may  be  difficult  in  cases  in  which 
evidence  of  thrombosis  of  peripheral  veins  is  lacking.  There  is 
likely  to  be  pain  in  the  side  and  cough  with  bloody  sputum.  Dyspnea 
and  cyanosis  may  be  a  striking  feature  if  a  large  branch  of  the  pul- 
monary artery  is  plugged.  When  such  symptoms  occur  in  the  course 
of  cardiac  decompensation,  uterine  sepsis,  with  or  without  relation 
to  childbirth,  following  laparotomy  for  abdominal  sepsis,  otitis  media 
or  mastoid  disease  complicated  by  sinus  thrombosis  and  after  injuries 
to  the  extremities,  pulmonary  infarction  should  be  suspected.  Atten- 
tion to  the  order  in  which  the  symptoms  appear  may  make  a  probable 
diagnosis  possible.  Bloody  sputum  may  appear  within  a  few  hours 
or  be  delayed  for  two  to  three  days.  The  blood  may  be  in  the  form 
of  bloody  streaks,  but  is  more  commonly  intimately  mixed  and  of 
a  dark-red  color.  Particles  of  sputum  washed  in  bouillon  or  sterile 
salt  solution  may  show  no  bacteria  in  stained  preparations  or  in 
culture.  Chill  at  onset  is  at  times  observed,  but  less  often  than  with 
pneumonia.  Unlike  pneumonia,  the  temperature  does  not  rise  at 
once  with  the  onset  of  symptoms,  but  more  gradually,  and  reaches 
its  maximum,  which  seldom  exceeds  103°  only  after  a  day  or  two. 
In  some  cases  a  musty  odor  may  be  detected  in  the  breath.  On 
examination  the  signs  of  consolidation  and  consonating  rales  may 
be  found  at  one  or  both  bases.    Dry  pleurisy  or  pleurisy  with  effusion 


218  DISEASES  OF  THE  LUNGS 

may  he  present.  A  moderate  leukocytosis  is  often  observed.  In 
cases  terminating  favorably,  the  temperature  falls  by  lysis  and  the 
physical  signs  slowly  disappear.  It  is  not  uncommon  for  pulmonary 
infarction  to  occur  from  latent  venous  thrombosis  of  the  lower 
extremity  and  the  venous  involvement  become  manifest  some  time 
after  the  infarction  has  taken  place. 

Bronchopneumonia. — This  usually  presents  no  special  difficulty 
from  its  insidious  onset  during  the  course  or  at  the  conclusion  of 
other  conditions  in  which  it  occurs  as  a  complication,  patchy  and 
limited  involvement  of  one  or  both  lungs  and  termination  by  lysis 
in  favorable  cases.  Bronchopneumonia  occurs  chiefly  in  children  under 
one  year,  while  lobar  pneumonia  is  more  common  after  the  third 
year.  The  differentiation  of  lobar  from  confluent  bronchopneumonia 
in  which  the  physical  signs  are  the  same  may  be  impossible.  Atelectasis 
is  frequently  observed  in  the  course  of  bronchopneumonia  in  children 
and  at  times  in  adults,  but  the  signs  are  more  likely  to  suggest  a  pleural 
effusion  or  massive  rather  than  ordinary  lobar  pneumonia.  The  dul- 
ness,  diminished  or  absent  breathing,  voice,  whisper  and  tactile 
fremitus  over  the  atelectatic  area  are  inconstant,  and  may  be  made 
to  disappear  with  the  expulsion  by  cough  of  the  secretion  occluding 
the  bronchus  supplying  the  affected  territory. 

Pleural  Exudates. — In  typical  and  uncomplicated  cases  there  is  no 
difficulty.  In  primary  serofibrinous  pleuritis,  the  onset  is  more  often 
gradual  than  sudden,  and  an  initial  chill  is  rare,  though  chilliness 
is  common.  In  the  more  exceptional  cases  the  onset  is  abrupt,  with 
chill,  fever,  and  pain  in  the  side,  but  usually  no  bloody  sputum. 
Over  the  effusion  there  is  dulness  or  flatness,  diminished  bronchial 
or  absent  breathing,  and  diminished  or  absent  voice,  whisper  and 
tactile  fremitus.  When  the  exudate  is  of  sufficient  amount,  the  heart 
is  displaced  awray  from  the  effusion.  Dulness  in  the  paravertebral 
region  on  the  affected  side  is  greater  in  degree  with  an  effusion  than 
with  pneumonia,  and  Grocco's  paravertebral  triangle  of  dulness  may 
be  demonstrable  on  the  unaffected  side.  In  the  region  posteriorly 
just  above  an  effusion  occupying  the  base  of  the  pleural  sac,  there 
are  the  signs  of  consolidation,  dulness,  bronchial  breathing  and 
increase  of  voice,  whisper  and  tactile  fremitus.  These  signs  are  due 
to  retraction  or  compression  of  the  lung,  and  in  some  instances  of 
uncomplicated  effusion  they  extend  over  an  unusually  wide  area  and 
are  a  cause  of  confusion,  but  if  the  extreme  base  be  investigated  with 
care  the  presence  of  an  effusion  may  then  become  clear. 

On  the  other  hand,  atypical  pneumonia  may  present  features 
suggestive  of  pleural  effusion.  Cough  and  rusty  sputum  may  be  absent 
and  the  signs  equivocal.  The  breathing  may  be  suppressed  and  only 
faintly  or  not  at  all  bronchial.  Rales  may  be  absent,  and  the  voice, 
whisper  and  tactile  fremitus  diminished.  In  massive  pneumonia 
the  signs  are  those  of  effusion,  and  in  the  absence  of  bloody  sputum 
an   immediate   decision   may   be   impossible.     The   contour   of  the 


LOBAR  PNEUMONIA  219 

affected  region  may  be  unlike  that  with  effusion,  and  a  zone  of  reso- 
nance may  be  detected  between  the  lower  limit  of  the  affected  region 
and  the  base  of  the  lung.  In  pneumonia  affecting  the  extreme  base 
and  of  considerable  extent,  a  paravertebral  zone  of  relative  resonance 
may  be  determined  on  the  affected  side,  due  to  compensatory 
emphysema  of  the  unaffected  lung.  Grocco's  triangle  of  dulness  is 
absent.  If  the  bronchi  can  be  freed  of  secretion  by  cough,  the  signs 
of  consolidation  may  then  appear.  Dislocation  of  the  heart  is  in 
favor  of  an  effusion,  but  cardiac  displacement  may  not  be  demon- 
strable with  small  effusions,  and  in  doubtful  cases  exploratory 
puncture  should  not  be  delayed. 

Persistence  of  Fever  After  the  Time  of  its  Expected  Decline  or  Reelevation 
of  Temperature  After  Defervescence. — It  is  well  to  have  in  mind  the 
causes  of  a  protracted  course  or  a  febrile  disturbance  after  deferves- 
cence. The  explanation  will  usually  be  found  in  serofibrinous  or 
purulent  pleurisy,  migratory  pneumonia,  organizing  pneumonia,  or 
otitis  media.  Less  often  pulmonary  abscess  or  gangrene,  peri- 
carditis, endocarditis,  phlebitis,  meningitis  or  peritonitis  may  be 
responsible. 

Prognosis. — Pneumonia  is  always  to  be  regarded  as  serious,  and 
even  under  the  most  favorable  conditions  threatens  life  in  a  con- 
siderable proportion  of  the  cases.  Of  465,400  cases  collected  from 
the  literature  by  Wells,  94,826  died,  a  mortality  of  20.4  per  cent.  In 
all  large  series,  the  mortality  usually  ranges  from  20  to  26  per  cent. 
Of  2025  cases  at  the  Massachusetts  General  Hospital  (1897  to  1913), 
5071  (25  per  cent.)  died.  The  lowest  mortality  in  any  one  year  was 
20  (15.3  per  cent.)  among  130  cases  in  1906  and  the  highest  38 
(31.6  per  cent.)  among  120  cases  in  1899.  In  a  series  of  500  cases, 
the  largest  number  of  consecutive  recoveries  was  16.  The  mortality 
is  lower  in  private  than  in  hospital  practice. 

The  influence  of  sex  is  shown  in  practically  all  large  series,  the 
mortality  being  lower  for  men  than  for  women.  Of  46,278  cases 
collected  by  Musser  and  Norris  with  a  mortality  of  21.1  per  cent., 
33,351  were  males  with  6449  (19.3  per  cent.)  deaths  and  12,927  were- 
females  with  3431  (26.9  per  cent.)  deaths. 

Age. — Youth  is  a  favorable  factor.  Jurgensen2  had  only  4  deaths 
among  110  cases  during  the  first  ten  years  of  life.  Barthez3  had  only 
2  deaths  in  212  children  from  two  to  fifteen  years  of  age.  In  the 
collected  statistics  of  Frankel  the  mortality  from  the  sixth  to  the 
twentieth  year  did  not  exceed  6.4  per  cent.;  from  the  twenty-first 
to  the  thirtieth  year,  14.8  per  cent.;  from  the  thirty-first  to  the 
fortieth  year,  26.4  per  cent.;  from  the  forty-first  to  the  fiftieth  year, 
39.3  per  cent.,  and  from  the  fifty-first  to  the  sixtieth,  43.1  per  cent. 
Over  sixty  the  mortality  may  rise  as  high  as  65  per  cent. 

1  Children  comprise  only  a  small  proportion  of  the  total  admissions. 

2  Ziemssen's  Handb.  d.  spec.  Path.  u.  Ther.,  1874,  v,  137. 

3  Quoted  from  Jurgensen,  loc.  cit. 


220  DISEASES  OF   THE   LUXCS 

Personal  Condition. — -The  condition  of  bodily  health  and  the  previous 
habits  are  of  chief  importance  in  determining  the  outlook.  Debilitated 
individuals,  those  with  chronic  disease  or  obesity,  and  alcoholics 
are  especially  liable  to  succumb.  Of  500  cases  at  the  Massachusetts 
General  Hospital,  122  died,  a  mortality  of  24.4  per  cent.  If  from 
among  the  fatal  cases  those  who  used  alcohol  to  excess  (28),  those 
with  chronic  circulatory  disease  (14),  with  acute  or  chronic  nephritis 
(5),  diabetes  (2),  pernicious  anemia  (2),  lymphatic  leukemia  (1), 
typhoid  fever  (1),  cancer  of  the  stomach  (1),  pulmonary  tuberculosis 
(1),  diphtheria  (1),  asthma  and  bronchitis  (2),  progressive  muscular 
atrophy  (1),  pregnancy  (1),  inguinal  hernia  (1),  and  those  remaining 
cases  without  obvious  complication,  but  fifty  years  of  age  or  over 
(15)  be  omitted,  the  number  of  deaths  which  can  be  ascribed  to 
pneumonia  or  its  complications  is  reduced  to  46,  a  mortality  of  9.2 
per  cent.  In  Osier's1  series  of  100  autopsy  cases,  25  showed  extensive 
interstitial  changes  in  the  kidneys.  The  mortality  is  low  in  vigorous, 
healthy  adults.  The  statistics  given  by  Frankel2  from  the  Imperial 
Prussian  Army  indicate  how  low  the  mortality  may  be  in  healthy, 
picked  men.  Among  85,000  cases  occurring  from  1878  to  1898,  the 
mortality  was  only  between  3.1  and  4.3  per  cent.;  in  the  Austrian 
Army  from  1891  to  1896,  5.8  per  cent.,  and  in  the  French  Army  8 
per  cent. 

Character  of  the  Organisms. — Concerning  the  influence  of  the  type 
of  organisms  too  little  is  yet  known  to  permit  of  definite  statements. 
Lobar  pneumonia  due  to  typical  pneumococci  is  mild  in  comparison 
to  that  due  to  Friedlander's  bacillus.  The  outlook  in  pneumonia 
due  to  the  streptococcus  mucosus  capsulatus  appears  to  be  less 
favorable  than  that  due  to  typical  pneumococci,  and  this  group  thus 
appears  to  stand  between  pneumococcus  and  Friedlander's  bacillus 
pneumonia  in  seriousness. 

Complications. — Meningitis  is  the  most  serious  and  is  always  fatal. 
Acute  endocarditis  adds  greatly  to  the  gravity  of  the  situation  and 
acute  pericarditis,  though  less  serious  than  endocarditis,  endangers 
the  chances  of  recovery.  Serofibrinous  pleurisy  does  not  appreciably 
increase  the  mortality.  Empyema  is  more  dangerous  and  fewer  cases 
recover  when  thus  complicated.  Abscess  and  gangrene  are  grave 
complications. 

Other  Factors. — The  presence  of  leukocytosis  is  of  little  value  in 
estimating  the  prognosis,  but  its  absence  is  an  unfavorable  sign. 
The  mortality  varies  with  the  extent  of  pulmonary  involvement, 
being  higher  in  proportion  to  the  number  of  lobes  affected,  and  in 
the  presence  of  a  spreading  infection.  Extremes  of  temperature,  such 
as  hyperpyrexia  or  subnormal  temperature,  are  of  unfavorable  import. 
As  already  noted,  from  a  third  to  a  half  of  adults  with  a  pulse  rate 
of  120  or  over  and  about  three-quarters  of  those  with  a  rate  of  140 

1  Practice  of  Medicine,  1905,  p.  188.  2  Loc.  cit. 


LOBAR  PNEUMONIA  221 

or  over  succumb.  Cardiac  arhythmia  is  to  be  feared.  Persistence 
of  pneumococci  in  the  blood  in  the  latter  part  of  the  illness,  subjective 
dyspnea,  respiration  rate  above  50  in  adults,  extreme  cyanosis  or 
pallor  and  cyanosis,  weakness,  cold  and  clammy  extremities,  per- 
sistent insomnia,  delirium,  and  coma  are  to  be  regarded  as  unfavor- 
able. But  estimation  of  the  chances  of  recovery  are  at  best  uncertain 
in  individual  cases.  Cases  in  which  from  the  apparent  mildness  of 
the  symptoms  the  outlook  appears  to  be  favorable  may  take  a  sudden 
turn  for  the  worse,  and,  on  the  other  hand,  a  condition  of  great 
gravity  may  terminate  favorably.  The  mortality  in  those  who  have 
previously  had  pneumonia  is  somewhat  lower  than  the  average.  The 
death  rate  in  negroes  is  higher  than  in  whites.  High  altitude  has 
been  thought  to  increase  the  death  rate  from  pneumonia,  but  statistics 
do  not  show  that  it  is  a  factor  of  importance.  Brewer1  concluded, 
from  a  study  of  the  statistics  for  the  United  States  Army  from  July  1, 
1870,  to  June  30,  1874,  that  altitude  has  nothing  to  do  with  the 
mortality  from  lobar  pneumonia. 

Death. — This  usually  comes  on  gradually  in  pneumonia  and  with 
increasing  symptoms  of  toxemia.  In  rare  instances,  the  patient  may 
be  overwhelmed  by  the  infection  and  die  within  two  to  three  days 
of  the  onset,  but  the  fatal  termination  is  usually  delayed  until  the 
fifth  to  the  tenth  or  eleventh  day  and  may  not  occur  for  several  weeks. 
The  temperature  is  usually  elevated  to  the  end,  but  at  times  falls 
to  normal  or  subnormal  as  the  end  approaches.  The  degree  of  the 
toxemia  is  usually  independent  of  the  height  of  the  temperature  and 
the  extent  of  the  pulmonary  involvement.  Interference  with  respira- 
tion and  cardiac  failure  are  of  less  importance  in  the  majority  of 
cases  than  the  results  of  the  general  infection,  but  nevertheless  play 
a  more  important  part  than  in  other  infections  in  which  the  pulmonary 
involvement  is  less  extensive  and  more  gradual  in  development. 
At  times  cardiac  failure  is  a  prominent  feature  as  indicated  by  the 
degree  of  cyanosis,  weakness  and  irregularity  of  the  pulse,  edema 
of  the  otherwise  unaffected  parts  of  the  lungs  and  engorgement  of 
the  right  side  of  the  heart.  Exhaustion  of  the  vasomotor  centre 
has  long  been  thought  to  be  an  important  factor  in  fatal  cases. 
Porter  and  Newburgh2  conclude  from  experiments  in  animals  near 
death  from  pneumonia  that  the  evidence  for  impairment  of  the  vaso- 
motor apparatus  is  inconclusive.  Sudden  death  may  occur  during 
the  course  of  the  disease  or  after  convalescence  is  established  and 
recovery  seems  assured.  In  such  cases  the  cause  of  death  is  usually 
cardiac  or  pulmonary  thrombosis.  In  two  cases  in  this  series,  sudden 
death  occurred  on  the  second  and  eighth  day  of  convalescence  respect- 
ively and  at  autopsy  pulmonary  embolism  was  found  in  one  and 
pulmonary  thrombosis  in  the  other. 

1  Southern  California  Prac,  1906,  xxi,  607. 

2  Boston  Med.  and  Surg.  Jour.,  January  22,  1914. 


222  DISEASES  OF  THE  LUNGS 

Prophylaxis. — The  pneumococeus  must  be  regarded  as  maintaining 
its  existence  by  transfer  from  person  to  person  and  the  respiratory 
tract  is  the  usual  channel  of  infection.  Transfer  of  the  virus  by 
contact  with  moist  sputum,  droplet  infection  or  the  inhalation  of 
material  which  through  drying  has  contaminated  the  air  is  probably 
the  common  mode  of  transmission.  Contact  with  utensils  which  have 
been  used  by  persons  who  harbor  the  organism  is  another  source  of 
danger.  Contamination  of  the  air  about  an  infected  individual  occurs 
when  particles  of  sputum  containing  pneumococci  are  expelled  by 
sneezing,  coughing  or  talking.  Indirect  transfer  through  water,  soil, 
food  or  intermediate  host  is  unlikely.  The  problem  of  prevention 
is  complicated  by  the  fact  that  the  pneumococeus  is  found  in  the 
saliva  of  a  considerable  proportion  of  healthy  individuals,  as  well 
as  in  those  suffering  from  acute  respiratory  infection. 

General  measures  concerning  which  the  public  must  be  educated 
apply  as  well  to  ordinary  "colds,"  influenza,  tuberculosis,  diphtheria, 
whooping  cough,  and  many  other  diseases  as  to  pneumonia.  Cleanli- 
ness in  its  broadest  sense  and  including  freedom  from  pathogenic 
bacteria  in  places  where  they  can  gain  entrance  to  the  body  must 
be  secured  with  such  discrimination  as  a  knowledge  of  sources  of 
infection  and  modes  of  communication  will  afford.  The  value  of 
fresh  air  and  sunshine  as  disinfectants  should  be  understood  by  all. 
Regulations  forbidding  expectoration  in  public  places  should  be 
enforced,  as  much  for  the  purpose  of  creating  public  opinion  against 
a  dangerous  and  obnoxious  practice  as  for  diminishing  the  spread 
of  disease  from  individual  cases.  The  carriers  of  pneumococci  are 
infinitely  more  numerous  than  patients  with  pneumonia.  Every 
individual  should  know  that  his  sputum  may  be  a  danger  to  others, 
and  if  allowed  to  dry  may  be  capable  of  spreading  disease.  The 
sputum  is  more  dangerous  in  the  presence  of  acute  or  chronic  respi- 
ratory infection,  and  should  be  expectorated  carefully  into  a  special 
receptacle  to  avoid  soiling  the  beard  or  moustache.  In  coughing  or 
sneezing,  expelled  particles  of  sputum,  which  may  give  rise  to  droplet 
infection,  should  be  caught  in  a  piece  of  cloth  placed  in  front  of  the 
mouth.  This  cloth  should  be  burned.  The  fingers  should  not  be 
moistened  in  the  mouth  in  turning  the  leaves  of  books,  public  docu- 
ments, etc.  The  rooms  of  patients  with  acute  respiratory  infection 
should  be  dusted  with  a  damp  cloth  and  swept  with  a  damp 
broom.  An  infected  individual  should  sleep  alone.  All  patients 
with  cough  and  expectoration  coming  to  polyclinics  or  seen  in  private 
practice  should  be  warned  against  the  danger  of  transferring  infectious 
material  from  person  to  person  with  the  same  care  that  is  recommended 
for  tuberculosis.  Such  instructions  will  not  only  serve  to  limit  the 
spread  of  disease  by  the  patients  themselves,  but  will  have  an  educa- 
tional value  in  the  community. 

Patients  with  pneumonia  should  be  isolated,  and  those  who  care 
for  them  should  see  that  proper  precautions  are  taken  against  dis- 


LOBAR  PNEUMONIA  223 

semination  of  pneumococci.  The  more  immediate  the  contact  with 
the  patient  the  greater  is  the  danger.  If  complete  isolation  is  impos- 
sible, the  patient's  bed  should  be  screened.  Every  effort  should  be 
made  to  prevent  drying  of  the  sputum  and  contamination  of  the  air. 
Contamination  of  the  clothing  or  bedding  should  as  far  as  possible 
be  avoided.  Soiled  bed  or  body  linen  should  be  immediately  removed, 
shaken  as  little  as  possible  in  handling,  and  boiled  for  one-half  hour 
before  it  is  sent  to  the  laundry.  Care  should  be  taken  by  those  in 
attendance  not  to  carry  infectious  material  to  the  mouth.  Patient's 
thermometers  and  utensils  for  food  should  be  kept  separate  and  the 
latter  boiled  after  use.  Persons  debilitated  by  age,  alcoholism,  or 
chronic  disease  should  avoid  contact  with  or  proximity  to  patients 
with  pneumonia.  Rooms  which  have  been  occupied  by  patients  with 
pneumonia  should  be  thoroughly  cleaned  and  disinfected. 

The  safest  method  of  disposal  of  the  sputum  is  cremation.  Carbolic- 
acid  (5  per  cent.)  is  probably  the  most  efficient  of  the  ordinary  dis- 
infectants and  should  be  left  in  contact  with  the  expectoration  for 
twenty-four  hours. 

The  influence  of  exposure  to  cold  and  chilling  of  the  body  in  pre- 
cipitating an  attack  of  pneumonia  is  uncertain,  but  worthy  of  atten- 
tion. The  danger  seems  to  be  greater  in  the  presence  of  an  acute 
respiratory  infection.  The  subjects  of  such  an  infection  should 
be  warned  against  exposure  to  cold  when  insufficiently  clad,  over- 
heated or  physically  tired.  Some  protection  may  be  afforded  those 
subject  to  "colds"  by  woolen  underwear  and  an  effort  to  increase 
individual  resistance — sleeping  with  the  window  open,  spending  much 
time  in  the  open  air  and  cool  morning  baths  followed  by  friction. 
A  good  reaction  should  be  obtained  after  the  bath.  The  hardening 
process  had  best  not  be  begun  in  cold  weather. 

The  greater  incidence  of  pneumonia  as  well  as  other  acute  respiratory 
infections  during  the  winter  months  is  probably  due  to  a  number  of 
causes,  the  relative  importance  of  which  is  difficult  to  estimate.  The 
tendency  to  live  more  within  doors  in  crowded  and  poorly  ventilated 
rooms  is  probably  a  factor.  The  greater  amount  of  dust  and  less 
abundant  sunshine  may  also  be  of  importance.  Infected  dust  is 
probably  concerned  in  dissemination  of  the  pneumococcus,  and 
municipal  authorities  should  take  immediate  steps  to  diminish  the 
amount  of  dust  and  smoke  in  the  cities. 

Since  overcrowding  is  an  important  factor  in  contagion  in  pneu- 
monia, as  in  other  infectious  diseases,  the  proper  regulation  of  housing 
conditions  is  a  necessary  measure  for  prevention. 

Preventive  Inoculation. — The  protective  value  of  inoculations  with 
the  pneumococcus  has  been  demonstrated  in  animals,  as  already 
noted  under  Immunity.  Whether  man  can  be  successfully  immunized 
against  pneumococcus  pneumonia  by  this  means  cannot  yet  be  regarded 
as  settled.  The  method  deserves  an  extended  trial  and  may  well 
be  used  as  a  preventive  measure  when  in  any  community  pneumonia 


224  DISEASES  OF  THE  LUNGS 

is  unusually  prevalent.  It  is  desirable,  however,  that  evidence  for 
or  against  the  value  of  the  procedure  be  obtained  as  soon  as  possible, 
and  with  this  end  in  view  a  portion  of  the  group  of  persons  living 
under  precisely  similar  conditions  as  those  subjected  to  inoculation 
should  be  reserved  as  controls.  Preventive  inoculations  were  recom- 
mended among  the  miners  on  the  Hand  by  Wright.  The  experience 
at  the  Premier  Mine  in  1913  was  promising.  In  1912,  among  17,000 
inoculated,  the  death  rate  from  pneumonia  was  6.89  per  thousand, 
while  among  6700  controls  the  death  rate  was  17.72  per  thousand.1 

Treatment. — Specific  Measures. — There  is  thus  far  no  specific  treat- 
ment for  pneumonia.  Drugs,  immune  sera,  vaccines,  and  leukocytic 
extracts2  have  not  yet  been  shown  to  be  of  definite  value.  Irritating 
drugs  injected  into  the  subcutaneous  tissue  to  cause  the  so-called 
"abscess  of  fixation"  and  promote  leukocytosis3  have  not  proved 
effective. 

Chemotherapy. — Experiments  with  derivatives  of  quinine  offer  some 
hope  of  successful  medication  in  pneumonia.  Since  Morgenroth 
and  Levy's4  first  publication  on  experimental  chemotherapy  in  pneu- 
mococcus  infections,  further  investigations  have  been  made  with 
ethylhydrocuprein,  with  which  mice  can  be  protected  against  subse- 
quent infection  with  pneumococci,5  and  cured  in  50  per  cent,  of  the 
animals  treated  six  hours  after  the  onset  of  the  infection  (Morgenroth 
and  Levy),  and  in  some  cases  even  as  long  as  twenty  hours  after 
infection;6  Wright7  demonstrated  bactericidal  action  of  ethylhydro- 
cuprein on  the  pneumococcus  in  vitro,  in  dilution  of  1  to  400,000  in 
twelve  hours,  and  Tugendreich  and  Rosso8  in  dilution  of  1  to  64,000 
in  two  hours  at  room  temperature.  A  dilution  of  1  to  256,000  at 
37°  did  not  prevent  the  growth  of  pneumococci  but  diminished  the 
virulence.  Pneumococci  become  resistant  against  the  drug,  both  in 
the  animal  body  and  in  vitro,  when  exposed  to  its  action  in  insufficient 
amount  to  exert  bactericidal  effects.  Frankel9  tested  the  effect  of 
the  drug  in  21  cases  of  pneumonia.  There  were  4  deaths.  Amblyopia 
occurred  in  3,  but  disappeared  after  the  drug  was  stopped.  Wright10 
used  it  in  8  cases.  Amblyopia  was  observed  in  2.  Vetlesen11  used  it 
in  9  cases,  all  of  whom  recovered,  and  Parkinson12  in  8  cases  with  2 
deaths.  Thus  far  no  definitely  favorable  action  has  been  shown  in 
man. 

1  Gorgas,  Jour.  Amer.  Med.  Assoc,  1914,  lxii,  p.  1855. 

2  See  His,   Jour.   Med.    Research,    1908,  xiv,   323:    Floyd    and  Lucas,   Jour.    Med. 
Research,  1909-10,  vol.  xxi. 

3  Fochier,  Dieulafoy's  Text-book  of  Medicine,  1911,  p.  139. 

4  Berl.  klin.  Woch.,  1911,  Nos.  34  and  44. 

5  Gutmann,  Zeit.  f.  Immunitatsforsch.,  1912,  1  Th.,  15,  orig.,  p.  625. 

6  Morgenroth  and  Kaufmann,  ibid.,  June  7,  1913. 

7  Lancet,  December  14  and  21,  1912. 

8  Zeit.  f.  Immunitatsforsch.  und  exp.  Ther.,  August  30,  1913,  1  Th.,  orig. 

9  Berl.  klin.  Woch.,  1912,  p.  664.  10  Loc.  cit, 
»  Berl.  klin.  Woch.,  August  11,  1913. 

12  Zeit.  f.  Chemotherapie  u.  verwandte  Gebiete,  1  Th.,  orig.,  Bd.  ii,  H.  1. 


LOBAR  PNEUMONIA  22;") 

Immune  Sera. — This  offers  the  greatest  promise,  but  as  yet  no  con- 
vincing results  have  been  published.  Failure  of  previous  attempts  to 
cure  by  this  means  may  have  been  due  to  the  use  of  antipneumococcic 
serum  without  immune  principles  against  the  infection  treated.  Cole1 
finds  that  of  72  cases  observed  at  the  Rockefeller  Institute,  the 
mortality,  according  to  the  type  of  the  infecting  organism,  was  as 
follows:  Of  34  cases  in  Group  I,  8  (24  per  cent.)  died;  of  13  cases  in 
Group  II,  8  (61  per  cent.)  died;  of  10  cases  in  Group  III,  6  (GO  per 
cent.)  died;  of  15  cases  in  Group  IV,  1  (6.6  per  cent.)  died.  By  the 
use  of  homologous  antipneumococcic  serum  in  a  further  series  of  cases 
in  Groups  I  and  II,  the  following  results  were  obtained:  Of  15  cases 
in  Group  I,  1  (6.6  per  cent.)  died,  and  of  8  cases  in  Group  II,  2  (25 
per  cent.)  died.  The  number  of  cases  is  too  small  for  fair  judgment 
concerning  the  efficiency  of  the  treatment,  but  the  method  is  more 
hopeful  in  other  respects  than  in  reduction  of  mortality.  Of  10  cases 
with  positive  blood-cultures,  the  blood  was  found  to  be  sterile  after 
the  first  injection  of  serum,  and  protective  substances  could  be  demon- 
strated in  the  blood  shortly  after  the  administration  of  the  serum  even 
when  it  was  given  early  in  the  disease. 

Vaccines. — The  prevention  of  infection  by  the  use  of  dead  or  living 
organisms  as  vaccines  is  already  established  for  certain  diseases, 
but  vaccines  have  never  been  shown  to  be  definitely  effective  against 
an  existing  infection.  Rosenow  and  Hektoen2  treated  146  cases  with 
partially  autolyzed  pneumococci,  using  148  cases  as  controls.  Of  the 
injected  group,  34  (23.3  per  cent.)  died,  and  of  the  uninfected  group, 
56  (37.8  per  cent.). 

General  Considerations. — Statistical  inquiries  on  pneumonia  in 
various  parts  of  the  world  have  shown  that  the  course  and  outcome 
of  the  disease  are  uninfluenced  by  venesection,  epistaxis,  wet  cup- 
ping, such  drugs  as  antimony,  mercury,  the  iodids,  veratrum  viride, 
quinin,  digitalis,  salicylic  acid,  phenacetin,  antipyrin,  creosote,  etc., 
or  catharsis,  diaphoresis,  diuresis,  inhalations,  insufflations,  hydro- 
therapy, and  special  diets.  At  present,  the  infection  is  beyond  our 
control  other  than  by  such  simple  measures  as  tend  to  spare  and 
support  the  strength  of  the  patient  by  careful  hygiene  and  nursing 
and  the  alleviation  of  symptoms.  A  recognition  of  the  ineffectiveness 
of  our  efforts  should  not  lead  to  the  relaxation  of  vigilance,  and  lives 
may  undoubtedly  be  saved  by  such  simple  means  as  are  already  in 
our  possession,  more  particularly  in  those  cases  in  which  there  is  a 
balancing  between  life  and  death,  and  the  utmost  care  may  turn  the 
scale  in  the  right  direction.  Solicitous  relatives  and  friends  should 
be  made  to  understand  that  careful  hygiene  and  nursing  are  of  first 
importance  and  that  their  cooperation  will  be  of  assistance  in  prevent- 
ing physical  and  mental  fatigue  and  in  affording  encouragement 
when  needed.     Useless  medication  is  to  be  avoided.     The  toxemia 

1  The  Harvey  Lecture,  New  York,  December  12,  1913. 

2  Jour.  Amer.  Med.  Assoc,  December  20,  1913,  p.  2203. 
15 


226  DISEASES  OF  THE  LUNGS 

may  be  favorably  influenced  by  any  increase  in  the  resistance  of 
the  individual  obtained  by  these  measures  and  by  efforts  to  favor 
elimination.  It  is  therefore  advisable  to  furnish  an  abundant  supply 
of  liquids  and  especially  water.  In  severely  toxic  cases,  enemata  of 
water  given  by  the  drop  method  may  be  of  service. 

Examination  of  Patients. — A  daily  physical  examination  should 
ordinarily  be  made  by  the  physician.  The  pulmonary  lesion  should 
be  investigated  and  an  estimate  made  of  the  degree  of  infection  and 
toxemia.  For  the  examination  of  the  posterior  thoracic  regions  the 
patient  may  be  turned  on  his  side,  all  exertion  on  his  part  being  avoided 
during  the  procedure.  Cough  is  less  often  excited  if  he  is  turned  on 
the  affected  side.  The  windows  should  be  closed  before  the  patient 
is  exposed,  and,  if  necessary,  perspiration  should  be  wiped  from  the 
skin.  In  patients  who  are  desperately  ill  the  likelihood  of  obtaining 
valuable  information  by  an  examination  of  the  back  must  be  weighed 
against  the  exertion  and  discomfort  to  which  the  patient  may  be 
subjected  by  the  change  of  position,  but  it  is  usually  safer  to  investi- 
gate this  region  for  a  complicating  pleural  effusion  than  to  waive  this 
part  of  the  examination.  Throughout  the  course  of  the  illness  the 
physician  should  constantly  be  on  the  watch  for  complications.  Pleural 
or  pericardial  effusion,  phlebitis,  acute  dilatation  of  the  stomach, 
abdominal  distention,  a  full  bladder,  and  otitis  media  are  among  the 
conditions  against  which  prompt  and  appropriate  treatment  may  be 
of  great  importance. 

Hygienic  Management. — The  patient  should  of  course  be  abed. 
The  transfer  of  the  patient  to  a  hospital  is  to  be  judged  after  considera- 
tion of  the  facilities  at  home  and  the  danger  of  moving  the  patient. 
A  short  journey  by  ambulance  and  with  the  patient  in  the  reclining 
position  may  be  permitted  during  the  first  part  of  the  illness,  but  is 
inadvisable  at  the  height  of  the  disease  and  may  diminish  the  chances 
of  recovery. 

The  patient's  room  should  be  large  and  well  ventilated.  It  should, 
if  possible,  be  in  a  quiet  part  of  the  house.  An  open  fireplace  improves 
the  ventilation.  An  abundance  of  sunshine  and  fresh  air  is  desirable. 
The  windows  should  be  open,  and  if  dust  or  snow  is  troublesome, 
cheese-cloth  screens  will  afford  protection.  The  temperature  of  the 
room  should  be  kept  at  about  65°  F.,  and  the  heating  accomplished  if 
possible  by  an  open  fire.  If  necessary,  nurses  or  attendants  should 
wear  extra  clothing.  The  patient's  bed  should  be  single,  approachable 
from  both  sides,  and  sufficiently  high  to  make  attendance  on  the  patient 
by  physician  and  nurses  capable  of  performance  without  strain  to  the 
back.  The  mattress  should  be  firm  and  comfortable  and  protected  by 
rubber  and  draw-sheets.  The  bed  clothing  should  afford  sufficient 
protection  against  cold,  but  should  not  be  heavy  enough  to  impede 
respiration  or  produce  sweating.  Short  woolen  nightshirt  or  pajamas 
are  desirable.    The  apparel  should  afford  ready  access  for  examination 


LOBAR  PNEUMONIA  227 

and  the  covering  for  the  chest  should  be  slit  up  the  whole  length  of  the 
front  and  fastened  with  buttons  or  other  means. 

Directions  for  Nurses. — The  patient's  strength  must  be  spared  by 
every  possible  means.  He  should  not  feed  himself,  but  should  be  fed 
by  the  nurse  with  as  little  exertion  on  his  part  as  possible.  During 
the  feeding  he  should  remain  in  the  recumbent  position.  Liquid 
nourishment  or  water  may  be  taken  from  a  glass  by  means  of  a  bent 
glass  tube.  All  unnecessary  excitement,  business  or  family  cares  and 
expressions  of  anxiety  should  be  avoided.  All  unnecessary  talking 
is  to  be  avoided  and  even  the  most  congenial  visitors  restricted  to  a 
short  visit  at  stated  intervals  and  cautioned  not  to  tire  the  patient. 
The  discharges  should  be  passed  into  the  urinal  or  bed-pan.  Straining 
at  stool  is  to  be  avoided.  Surface  bathing  may  be  given  once  a  day. 
The  windows  should  be  shut  and  the  room  warmed  before  the  bath 
is  given.  Needless  exposure  during  the  process  is  to  be  avoided  and  a 
part  of  the  body  should  be  washed  and  dried  before  other  parts  are 
exposed.  If  bathing  is  followed  by  fatigue,  it  may  be  omitted.  Hot- 
water  bags  or  bottles  or  an  electric  heater  may  be  used  if  necessary 
for  warmth  to  the  extremities.  Careful  attention  to  the  arrangement 
of  the  pillows  and  bed-rest  will  assist  the  patient  in  securing  a  comfort- 
able position,  which  should  be  occasionally  changed  to  diminish  the 
danger  of  hypostasis.  The  patient  should  not  be  allowed  to  sit  up. 
Changes  of  position  may  be  affected  by  moving  the  patient  from  his 
back  to  one  or  the  other  side.  The  twenty-four-hour  amount  of  urine 
should  be  measured  and  recorded.  Failure  to  pass  urine  after  a  period 
of  eight  hours  should  be  reported  to  the  physician.  Sufficient  sleep 
is  important,  and  it  is  usually  unnecessary  to  awake  the  patient  for 
either  food  or  medicine.  Temperature,  pulse  and  respiration  should 
be  recorded  every  four  hours  unless  the  patient  is  asleep.  The  tem- 
perature may  be  taken  by  rectum  if  the  thermometer  in  the  mouth 
is  disturbing.  A  chart  should  be  kept  of  the  character  and  amount 
of  nourishment.  Patients  with  pneumonia  should  never  be  left  alone. 
Sudden  and  unexpected  delirium  may  induce  the  patient  to  injure 
himself  or  others. 

Careful  attention  should  be  paid  to  the  patient's  mouth.  The  teeth 
should  be  brushed  twice  a  day.  A  mouth  wash  consisting  of  boracic 
acid  drams  4  (16  c.c.)  and  lemon  juice  and  glycerin  of  each  4  ounces 
(128  c.c.)  applied  every  four  hours  by  means  of  a  swab  of  cotton  rolled 
on  an  orange-wood  stick  is  of  service.  Dobell's  Solution  may  also  be 
used  as  a  spray. 

If  necessary  for  a  daily  evacuation,  a  suds  enema  may  be  given. 

The  sputum  should  be  disinfected.  Sputum  boxes  should  be  burned. 
If  the  patient  is  too  ill  to  expectorate  into  a  special  receptacle,  small 
pieces  of  gauze  or  linen  cloth  may  be  used  to  wipe  the  sputum  from  the 
lips.  These  may  be  placed  in  a  paper  bag  and  burned.  If  disinfection 
of  the  expectoration  is  accomplished  by  means  of  carbolic  acid  or 


228  DISEASES  OF  THE  LUNGS 

other  poisonous  material,  the  solutions  must  be  kept  in  some  place 
which  is  inaccessible  to  the  patient. 

Diet. — There  are  no  special  restrictions  and  the  patient  may  take 
as  much  of  simple  and  nutritious  food  as  he  can  digest.  As  the  appetite 
is  often  impaired,  the  diet  will  usually  consist  of  liquid  and  soft 
solid  food,  such  as  milk,  ice-cream,  custards,  eggs,  cereals,  broths, 
milk  toast,  crackers,  etc.  Liquid  food  is  best  given  every  two  hours, 
but  the  feedings  may  be  omitted  when  the  patient  is  asleep.  While 
it  is  desirable  to  maintain  the  strength  of  the  patient  by  nourishing 
food,  it  is  unwise  to  surpass  his  inclinations  in  regard  to  quantity, 
and  no  anxiety  need  be  felt  if,  as  usually  happens,  the  full  number  of 
calories  needed  by  a  person  in  health  cannot  be  maintained.  Attention 
must  be  paid  to  the  effect  of  the  diet  on  the  gastro-intestinal  tract. 
If  there  is  vomiting  or  flatus,  all  food  may  well  be  omitted  for  a  time. 
Tympanites  may  increase  the  dyspnea  by  elevation  of  the  diaphragm 
and  embarrassment  of  the  respiration  and  the  circulation. 

An  abundance  of  fluid  should  be  supplied.  Small  quantities  of 
water  should  be  offered  to  the  patient  at  frequent  intervals.  Iced  water 
may  be  taken  if  preferred,  and  lemonade,  orange  juice,  albumin 
water,  grape  juice,  cocoa,  tea  or  coffee. 

After  the  fever  has  subsided  and  convalescence  is  established,  the 
appetite  returns  and  a  liberal  diet  is  allowed. 

Treatment  of  the  Special  Symptoms. — Chill. — The  patient  should  be 
put  to  bed  between  wrarm  blankets  and  with  hot-water  bags  or  bottles 
at  the  feet.    A  hot  drink  may  be  given. 

Herpes. — This  does  not  usually  require  treatment.  If  troublesome, 
the  lesions  may  be  smeared  with  zinc-oxide  ointment. 

Fever. — This  is  the  result  of  infection  and  toxemia  and  cannot  be 
satisfactorily  combated  by  any  means  at  our  disposal.  The  use  of 
antipyretic  drugs  is  now  very  generally  abandoned.  Hydrotherapy 
may  be  employed  if  it  is  found  to  afford  symptomatic  relief.  There 
is  no  convincing  evidence  that  it  modifies  or  shortens  the  course  of  the 
disease  in  any  way,  but  in  some  cases  it  seems  to  quiet  the  nervous 
system  and  diminish  the  sense  of  ill-being.  Sponging  with  cool  water 
(75°  to  80°  F.)  limb  by  limb  and  the  trunk  by  section,  one  part  being 
dried  and  subjected  to  friction  before  proceeding  to  the  next,  may  be 
used  when  the  temperature  is  102.5°  or  more,  and  repeated  if  agreeable 
to  the  patient  every  four  to  six  hours.  The  windows  should  be  closed 
during  the  bath. 

Respiratory  System. — Pain  in  the  Side. — Local  friction  with  the 
hand,  the  application  of  the  ice-bag  or  Leiter's  coil,  hot-water  bottle 
or  electric  heater,  may  be  tried.  Fixation  of  the  side  by  means  of  a 
tight  thoracic  swrathe  may  be  successful.  Strapping  with  adhesive 
plaster  has  the  disadvantage  of  interference  with  chest  examinations 
and  may  lead  to  irritation  or  infection  of  the  skin.  Local  irritation 
with  iodin,  mustard  or  other  means,  and  the  use  of  wet  and  dry  cups 
and  leeches  may  only  add  to  the  patient's  discomfort,  and  are  to  be 


LOBAR  PNEUMONIA  229 

avoided.  If  simple  measures  do  not  suffice,  a  hypodermic  of  morphin 
may  be  given.  Morphin  is  one  of  the  most  valuable  drugs  in  pneumonia , 
and  there  should  be  no  hesitation  in  its  use  in  a  disease  which  rims 
so  short  a  course.  As  pain  may  prevent  sleep,  aggravate  the  dyspnea 
and  harass  and  fatigue  the  patient,  its  relief  is  important  to  conserve 
his  strength  and  enable  him  to  withstand  the  infection. 

Cough  and  Expectoration. — Cough  is  usually  necessary  for  the  expec- 
toration of  sputum,  and  an  effort  to  control  it  should  be  made  only 
for  some  definite  indication.  When  harassing  and  unproductive  cough 
disturbs  sleep,  aggravates  the  pain  in  the  side  or  tires  the  patient, 
codein  gr.  \  (0.016  gm.),  heroin  gr.  TV  (0.005  gm.)  or  a  subcutaneous 
injection  of  morphin  gr.  f  (0.008  gm.)  may  be  given.  When  the 
bronchial  secretion  is  abundant,  it  is  usually  best  not  to  give  morphin. 
If  the  expectoration  is  raised  with  difficulty,  ammonium  chlorid 
gr.  10  (0.650  gm.)  repeated  every  four  hours  may  be  of  service. 

Serofibrinous  and  Purulent  Pleural  Effusions. — The  differentiation 
between  serofibrinous  and  purulent  effusions  must  usually  be  settled 
by  exploratory  puncture  and  the  decision  concerning  the  appropriate 
treatment  made  after  examination  of  the  fluid.  The  indications  for 
treatment  are  considered  in  the  sections  on  Serofibrinous  and  Purulent 
Pleurisy. 

Abscess  and  Gangrene. — Treatment  of  these  complications  is  dis- 
cussed in  the  section  on  Abscess  and  Gangrene. 

Delayed  Resolution. — It  is  important  to  exclude  pleural  effusion, 
pulmonary  abscess  or  tuberculosis.  Until  the  causes  underlying 
delayed  resolution  are  better  understood,  chief  reliance  must  be  placed 
on  improvement  of  the  general  health  and  nutrition.  An  abundance 
of  food,  rest  and  fresh  air  are  of  most  importance.  External  applica- 
tions to  the  chest  and  drugs  internally  are  probably  ineffectual.  Edsall 
and  Pemberton1  applied  the  x-rays  with  apparent  success.  Fibrolysin 
has  been  used  in  2  cases  by  Krusinger,2  and  in  1  case  by  Brenner.3 
The  results  appeared  to  be  favorable. 

Cardiovascular  System. — Cardiac  Weakness. — This  is  but  one  feature 
of  the  general  effect  of  the  infection  and  toxemia  on  the  vital  organs 
of  the  body.  The  failure  of  the  circulation  is  more  readily  apparent 
than  that  of  other  systems,  and  this  has  led  to  undue  emphasis  on 
cardiac  failure  as  a  cause  of  death  in  pneumonia.  Cyanosis  as  a  measure 
of  failure  of  the  circulation  is  uncertain  on  account  of  other  factors 
as  a  cause.  Extensive  pulmonary  involvement  probably  embarrasses 
the  right  side  of  the  heart  to  some  degree,  but  cannot  be  held  account- 
able for  cardiac  failure  in  view  of  the  tolerance  which  the  heart  shows 
in  the  presence  of  equal  or  greater  interference  with  the  pulmonary 
circulation  in  pleurisy  with  effusion,  pneumothorax,  pulmonary  infarc- 
tion, etc.  and  the  usual  absence  of  evidences  of  right-sided  engorge- 
ment in  pneumonia.    In  cases  in  which  the  pulse  is  rapid,  weak  and 

i  Amer.  Jour.  Med.  Sci.,  February,  1907,  p.  286. 

2  Munch,  med.  Woch.,  1908,  No.  14.  3  Ibid.,  1913,  No.  28. 


230  DISEASES  OF  THE  LUNGS 

irregular,  the  second  pulmonic  sound  of  diminished  intensity,  the  first 

cardiat-  sound  enfeebled  and  the  lung'  shows  signs  of  pulmonary  edema, 
it  is  desirable  to  support  the  circulation  by  every  means  in  our  power. 

The  measures  already  suggested  under  hygienic  management  and 
directions  for  nurses,  especially  those  which  spare  the  patient's  strength, 
are  more  likely  to  prevent  the  development  of  cardiac  weakness  than 
any  other  means  at  our  command.  Cardiac  stimulants  are  uncertain 
and  far  less  important,  but  may  be  used  for  the  purpose  both  of  preven- 
tion and  relief.  Digitalis  in  doses  of  minims  10  (0.00  c.c.)  of  the  tinc- 
ture, gr.  1  (0.0G5  gm.)  of  the  powdered  leaves,  or  digipuratum  may  be 
administered  as  a  routine,  beginning  on  the  second  or  third  day  of 
the  disease.  With  the  development  of  signs  of  cardiac  weakness  the 
amount  of  digitalis  may  be  increased.  Digipuratum  may  be  admin- 
istered subcutaneously  or  intravenously.  Camphor,  gr.  1|  (0.0975  gm.) 
in  1  c.c.  of  sterile  oil,  may  be  given  intramuscularly,  and  caffein  in  the 
form  of  caffein  sodium  benzoate,  in  one-grain  doses,  every  two  to 
four  hours.  Strophanthin  intravenously  in  doses  of  a  half  to  1  mg.  is 
useful  in  some  cases.  It  should  never  be  given  in  large  doses  or  after 
digitalis  has  been  administered.  Strychnin,  nitroglycerin,  adrenalin 
chlorid,  spartein  sulphate,  and  musk  are  at  times  used.  They  are  of 
doubtful  value.  Alcohol  is  used  less  and  less  and  it  would  be  better 
if  it  were  not  used  at  all,  except  in  cases  of  chronic  alcoholism.  Persons 
previously  accustomed  to  the  excessive  use  of  alcohol  should  not  have 
their  supply  suddenly  withdrawn  during  an  attack  of  pneumonia  for 
fear  of  precipitating  delirium  tremens. 

Venesection  is  now  seldom  used,  and  only  when  the  indications 
point  to  severe  mechanical  embarrassment  of  the  heart.  Extreme 
cyanosis,  beginning  pulmonary  edema  and  dilatation  of  the  right 
side  of  the  heart  justify  its  consideration.  I  have  used  it  with  apparent 
benefit  in  a  few  cases  of  pneumonia  complicating  mitral  stenosis.  From 
300  to  500  c.c.  of  blood  may  be  removed.  As  a  means  of  combating 
toxemia,  venesection  is  an  irrational  procedure,  as  it  may  as  fairly  be 
argued  that  abstraction  of  blood  removes  protective  substances  as 
circulating  toxins. 

Acute  Endocarditis. — The  patient  should  be  abed  as  long  as  fever 
or  any  other  evidence  of  activity  of  the  endocardial  infection  persists, 
and  for  three  to  four  weeks  longer  in  order  that  the  heart  muscle  may 
have  time  to  adjust  itself  to  the  changed  conditions.  Even  then  he 
should  be  cautious  about  the  resumption  of  customary  exertion. 

Pericarditis. — Treatment  consists  in  the  application  of  cold  or  the 
administration  of  morphin  for  the  relief  of  pain.  Thoracentesis  should 
be  performed  when  an  effusion  is  present.  Serofibrinous  accumula- 
tions of  fluid  should  be  aspirated.  With  purulent  fluid  the  pericardium 
should  be  opened  and  drained. 

Phlebitis. — If,  as  usually  happens,  the  leg  veins  are  involved,  the 
patient  should  be  kept  absolutely  at  rest  to  favor  subsidence  of  the 
process  and  prevent  the  detachment  of  a  clot  and  pulmonary  embolism. 


LOBAR  PNEUMONIA  231 

The  affected  limb  should  be  supported  comfortably  on  a  pillow.  Mas- 
sage and  all  rough  handling  are  to  be  avoided.  The  leg  should  be 
kept  at  rest  for  at  least  a  month  and  longer  if  necessary. 

G astro-intestinal  Tract. — If  the  bowels  have  not  moved,  it  is  wise 
at  the  outset  to  administer  a  mild  cathartic,  as  sodium  phosphate, 
gr.  45  (2.925  gm.)  in  half  a  tumbler  of  lukewarm  water,  a  Seidlitz 
powder  or  saline  cathartic  water.  If  there  is  vomiting  or  flatus,  it  is 
well  to  largely  restrict  the  amount  of  nourishment  and  albumin  water 
alone  may  be  given.  Throughout  the  course  of  the  illness  it  is  important 
to  prevent  and,  if  necessary,  to  overcome  tympanites.  This  may  be 
accomplished  by  securing  a  daily  evacuation,  for  which,  if  needed, 
a  suds  enema  may  be  given.  If  tympanites  is  troublesome,  restriction 
in  the  amount  of  food,  turpentine  stupes,  enemata  and  the  rectal 
tube  may  be  employed.  Acute  dilatation  of  the  stomach  should  be 
kept  in  mind  as  a  cause  of  vomiting  and  abdominal  distention.  Treat- 
ment consists  in  passage  of  the  stomach  tube  and  the  evacuation  of 
gas  and  fluid  contents  and  lavage  until  the  wash-water  returns  clear. 
Food  and  drink  by  the  mouth  should  be  stopped.  If  the  patient  is 
turned  on  the  right  side  or  on  the  face,  the  tendency  to  mechanical 
obstruction  of  the  duodenum  may  be  prevented. 

Peritonitis. — This  should  be  treated  on  general  surgical  principles. 
The  outlook  in  the  diffuse  form  secondary  to  pneumonia  is  very  unfavor- 
able. Recovery  may  follow  incision  and  drainage  of  circumscribed 
collections  of  pus. 

Parotitis. — The  local  application  of  heat  or  cold  may  be  used  for 
the  relief  of  pain.  Morphin  may  be  used  if  necessary.  As  soon  as  the 
presence  of  pus  is  established,  the  gland  should  be  incised  and  drained. 

Acute  Nephritis. — This  should  be  treated  upon  the  same  principles 
as  apply  to  other  forms  of  acute  nephritis.  The  patient  should  be 
abed  with  flannel  nightshirt  and  between  blankets.  The  diet  should 
be  simple  and  contain  milk  to  an  amount  not  exceeding  a  quart  to  a 
quart  and  a  half  a  day.  Cream,  cereals  (oatmeal,  rice,  tapioca  and 
sago),  bread,  macaroni  and  custards  in  limited  amount  may  be  given. 
The  diet  should  be  arranged  so  as  not  to  contain  more  than  50  grams  of 
protein  during  the  acute  stages  of  the  disturbance.  A  moderate 
diminution  in  the  amount  of  salt  is  desirable.  Elimination  by  the 
bowel  should  be  favored  by  the  use  of  saline  cathartics,  but  active 
purgation  is  unnecessary  if  dropsy  and  uremic  symptoms  are  absent. 
Elimination  by  the  skin  may  be  secured  by  the  hot  pack  or  hot-air 
bath.  Water  is  the  best  diuretic  and  may  be  given  in  sufficient  amount 
to  satisfy  the  thirst  of  the  patient. 

Nervous  System. — Headache  is  usually  troublesome  only  in  the  early 
stages  of  the  disease,  and  may  then  be  treated  with  the  ice-cap,  or,  if 
severe,  with  phenacetin  gr.  5  (0.325  gm.)  combined  with  caffein  gr.  1 
(0.065  gm.).  Insomnia  due  to  pain  or  harassing  and  unproductive 
cough  may  be  relieved  with  morphin.  Sulphonal,  trional,  or  veronal 
may  be  used  in  the  absence  of  cardiac  weakness.    If  these  measures 


232  DISEASES  OF  THE  LUNGS 

fail,  hyoscin  hydrobromate  gr.  ,,',  „  to  •t,1,,,  (0. 00005  to  0.00032  gm.) 
may  be  tried.  Delirium  of  a  mild  type,  unassociated  with  cardiac 
weakness  and  beginning  pulmonary  edema,  has  usually  been  treated 
with  morphin  or  other  opium  derivative  or  chloral,  bromid  or  hyos- 
cin hydrobromate.  Alcoholic  cases  should  not  have  their  alcohol 
omitted  during  pneumonia.  In  cases  in  which  inanition  is  a  cause, 
especially  in  the  postcritical  delirium,  every  effort  should  be  made 
to  build  up  the  general  strength  with  nourishing  food  and  rest.  Forcible 
restraint  should  not  be  practised.  Depressant  drugs  should  as  far  as 
possible  be  avoided.1 

Meningitis  due  to  the  pneumococcus  has  thus  far  invariably  proved 
fatal.  The  success  obtained  in  the  treatment  of  meningitis  due  to  the 
meningococcus  of  Weichselbaum  by  means  of  intraspinal  injections 
of  antimeningococcic  serum  has  led  to  the  similar  use  of  antipneu- 
mococcic  serum  in  meningitis  due  to  the  pneumococcus.  No  favorable 
results  have  thus  far  been  reported.  This  seems  the  most  rational 
procedure  to  recommend,  and,  until  further  advances  have  been  made 
in  the  treatment  of  pneumococcic  meningitis,  deserves  a  further  trial. 

^icute  Otitis  Media. — This  is  common,  especially  in  children,  and  is 
frequently  overlooked.  Investigation  of  the  ears  should  be  made  a 
part  of  the  routine  physical  examination  in  pneumonia.  Suppurative 
otitis  media  should  be  treated  by  puncture  and  drainage  of  the  cavity. 
Early  detection  and  prompt  treatment  may  prevent  extension  to  the 
meninges  and  fatal  meningitis. 

Acute  Arthritis. — Simple  immobilization  with  or  without  aspiration 
may  be  sufficient  with  serofibrinous  effusions.  In  cases  in  which  the 
fluid  is  purulent,  the  joint  should  be  incised  and  drained.  All  unneces- 
sary manipulation  of  the  joint  structures  should  be  avoided. 

Pneumonia  and  Diabetes. — The  development  of  acidosis  is  to  be 
feared,  and  it  is  probably  safer  to  modify  or  abandon  the  restriction 
of  carbohydrates  at  once  with  the  onset  of  symptoms.  Milk  to  the 
amount  of  250  c.c.  every  two  hours  or  oatmeal  gruel  may  be  given. 
Sodium  bicarbonate  should  be  administered  in  sufficient  quantity 
if  possible  to  keep  the  urine  alkaline.  If  a  severe  grade  of  acidosis 
is  present,  as  much  as  100  grams  a  day  may  be  taken.  The  intake 
of  water  should  be  pushed  and,  if  necessary,  enemata  of  salt  solution 
given  by  the  drop  method.  If  coma  develops,  an  enema  of  10  per  cent, 
glucose  and  the  intravenous  injection  of  500  c.c.  of  3|  to  4  per  cent, 
sodium  carbonate  in  sterile  water  may  be  administered.  From  200  to 
400  c.c.  of  blood  should  be  removed  from  the  vein  before  the  intra- 
venous injection  is  made. 

1  Gregg  (Boston  Med.  and  Surg.  Jour.,  September  18,  1913)  reports  the  mortality 
in  delirium  tremens  in  five  large  general  hospitals  where  restraint  and  depressant  drugs 
were  used  as  26  per  cent.  At  the  Psychopathic  Hospital  in  Boston  with  eliminative 
treatment  by  continued  baths  and  packs,  Southard  (ibid.,  December  25,  1913)  finds 
the  mortality  3  per  cent,  in  64  cases.  These  results  apply  only  to  uncomplicated  cases, 
but  suggest  the  possibility  of  applying  similar  methods  of  treatment  to  complicated 
cases  and  among  them  pneumonia  with  delirium. 


LOBAR  PNEUMONIA  233 

Crisis. — The  crisis  is  usually  the  indication  of  a  decisive  victory 
won  by  the  patient  against  the  disease  and  little  more  need  be  expected 
of  the  physician  than  appropriate  words  of  congratulation.  But 
unfortunately  it  does  not  always  happen  that  the  patient  emerges 
unscathed  from  the  conflict.  In  some  cases  his  strength  is  spent, 
and  he  may  die  of  exhaustion  or  linger  for  a  time  between  life  and 
death.  The  watchfulness  of  those  in  attendance  must  therefore  not 
be  relaxed  at  this  period  of  the  illness,  and  the  patient's  strength  must 
still  be  spared  and,  if  necessary,  supported.  All  exertion  is  to  be 
avoided.  Hot  drinks,  warmed  blankets,  the  application  of  hot-water 
bags  or  bottles  and  cardiac  stimulation  may  be  necessary.  Compli- 
cations, especially  pleural  effusion,  must  be  carefully  sought  during 
the  epicritical  period.  The  patient  should  not  be  allowed  to  sit  up. 
An  abundance  of  food,  rest  and  sleep  are  important. 

Convalescence. — Rules  cannot  be  formulated  for  the  management 
of  convalescence.  If  the  patient's  strength  permits,  he  may  be  allowed 
to  get  up  at  the  expiration  of  about  a  week  after  the  termination  of  the 
disease.  Attention  to  the  diet,  suggestions  as  to  the  amount  and 
character  of  the  mental  or  physical  effort  permitted,  the  length  of 
time  which  should  elapse  before  the  resumption  of  customary  activities, 
vacation,  change  of  climate  and  other  matters  must  be  considered  with 
due  regard  to  the  needs  of  the  individual. 


CHAPTER  XL 
FRIEDLANDER'S  BACILLUS  PNEUMONIA. 

Friedlander's  bacillus  is  also  known  as  Friedlander's  bacillus  of 
pneumonia,  the  pneumobacillus,  and  bacillus  mucosus  capsulatus. 
Friedlander1  in  1883  reported  the  discovery  in  pneumonic  exudates 
of  an  organism  which  he  termed  the  pneumococcus.  Further  studies, 
especially  those  by  Weichselbaum,2  showed  this  to  be  an  encapsulated 
bacillus.  This  organism  is  occasionally  found  in  suppurative  lesions 
in  various  parts  of  the  body,  in  the  sputum  from  patients  with  simple 
bronchitis  and  in  the  sputum  and  pulmonary  exudate  from  cases  of 
bronchopneumonia.  In  rare  instances  it  is  found  as  the  apparent 
sole  cause  of  genuine  lobar  pneumonia. 

Occurrence. — Of  94  cases  of  croupous  pneumonia  in  Weichselbaum's 
series,  this  organism  was  found  in  5,  in  4  of  these  cases  by  culture. 
In  three  of  the  four  it  was  mixed  with  other  organisms.  E.  Frankel3 
found  two  Friedlander  pneumonias  among  77  cases  of  pneumonia. 
Of  192  cases  of  lobar  pneumonia  coming  to  autopsy  at  the  Massachu- 
setts General  Hospital,  this  organism  was  the  only  apparent  cause  in 
6.     (Autopsy  224,  328,  883,  1519,  2811,  and  3329.) 

Etiology. — In  smears  made  from  the  sputum  or  exudate  from  the 
lung,  the  pneumobacilli  appear  as  moderate-sized  rods  of  variable 
length.  They  are  usually  two  to  three  times  as  long  as  broad,  with 
rounded  ends.  At  times  they  are  found  in  pairs  or  short  chains.  A 
thick,  oval  capsule  can  be  demonstrated  about  the  organism  by  appro- 
priate methods  of  staining.  The  capsule  is  more  easily  demonstrable 
in  fresh  material  than  in  cultures.  The  organisms  decolorize  by  Gram's 
method  of  staining.  On  blood  serum  after  twenty-four  hours  in  the 
incubator,  translucent,  moist,  colorless,  confluent,  mucus-like  colonies 
appear.  The  colonies  are  viscid  and  can  be  drawn  out  into  threads  with 
the  platinum  wire.  The  water  of  condensation  may  be  cloudy  and 
viscid  in  consequence  of  the  growth.  Bouillon  is  clouded  and  a  thin 
pellicle  may  form.  The  organism  is  non-motile.  Spore  formation  is 
not  observed.  Glucose  agar  stab  cultures  show  growth  along  the  track 
of  the  inoculation  and  gas  production.  Gelatin  shows  a  grayish  white 
growth  along  the  line  of  inoculation  and  a  knob-like  growth  at  the  sur- 
face. Liquefaction  of  the  gelatin  does  not  take  place.  Litmus  milk 
is  acidified  and  coagulated.    On  potato  a  thin,  colorless,  viscid  growth 

1  Die  Mikrokokken  der  Pneumonie,  Fort.  d.  Med.,  1883,  Bd.  i,  No.  22. 

2  Med.  Jahrbiicher,  1886,  p.  483. 

3  Apelt,  Munch,  med.  Woch.,  April  21,  1908. 


FRIEDLANDER'S  BACILLUS  PNEUMONIA 


235 


takes  place.     Growth  occurs  both  at  room  temperature  and  in  the 
incubator. 

Inoculation  of  rabbits,  guinea-pigs  and  white  mice  usually  causes 
fatal  septicemia.     Subcutaneous  inoculation  of  rabbits  may  give  rise 


Fig.  33 


Fig.  34 


Friedlander  bacillus,  smear  from  culture. 


to  local  suppuration  without  septicemia.  At- 
tempts to  produce  experimental  lobar  pneu- 
monia in  animals  have  usually  failed.  Fried- 
lander1  produced  focal  pneumonia  and  pleuritis 
in  mice  by  injection  into  the  lung  and  inhala- 
tion of  bacilli  in  suspension.  Intrathoracic 
injection  of  guinea-pigs  and  dogs  gave  similar 
results,  but  these  animals  proved  less  suscep- 
tible. Rabbits  proved  insusceptible.  In  one 
dog  intrathoracic  injection  gave  rise  to  typical 
lobar  pneumonia.  Similar  experiments  have 
since  been  made  with  practically  the  same 
results. 

Relation  of  Friedlander's  Bacillus  to  Pneu- 
monia.— The  importance  of  this  organism  as 
a  cause  of  lobar  pneumonia  has  been  questioned.  It  is  not  very 
uncommon  to  find  it  mixed  with  pneumococci  in  the  sputum  during 
life  and  in  the  pneumonic  exudate  after  death  in  cases  of  lobar 
pneumonia,  and  in  such  instances  the  pneumococcus  may  be  regarded 
as  the  probable  primary  cause  and  the  pneumobacillus  as  a  secondary 
invader.  Reported  instances  of  lobar  pneumonia  in  which  this 
organism  is  found  as  the  apparent  sole  cause,  comprise  for  the  most 
part  autopsy  cases  in  which  it  may  be  assumed  that  the  infection  is 
terminal  and  secondary  to  the  pneumococcus.  The  well-recognized 
tendency  of  the  pneumococcus  to  die  out  or  be  overgrown  by  secondary 


Friedlander's  bacillus 
culture. 


1  Die  Mikrokokken  der  Pneumonie,  Fort.  d.  Med.,  1883,  Bd.  i,  p.  715. 


231  > 


DISEASES  OF  THE  LUNGS 


invaders  lends  support  to  this  point  of  view.    That  secondary  invasion 
with  this  organism  may  take  place  is  suggested  by  one  of  the  Massa- 


Fig.  'do 


Friedliinder's  bacillus  in  sputum. 
Fig.  3G 


Friedlander's  bacillus  in  pulmonary  exudate.      X  1500. 


FRIEDLANDER'S  BACILLUS  PNEUMONIA  237 

chusetts  General  Hospital  eases  (542-54).  Organisms  resembling 
pneumococci  were  found  in  enormous  numbers  in  the  sputum  on  the 
eighth  day  of  the  disease,  while  on  the  next  day  enormous  numbers 
of  Friedlander's  pneumobacilli  were  present.  No  autopsy  was  obtained. 
While  the  matter  cannot  yet  be  regarded  as  settled,  the  following 
considerations  tend  to  uphold  the  independent  existence  of  primary 
lobar  pneumonia  due  to  this  organism.  In  one  case  at  the  Peter  Bent 
Brigham  Hospital,1  a  woman  (No.  2226),  aged  sixty-six  years,  was 
admitted  in  the  afternoon  with  a  history  of  having  worked  as  a  domestic 
until  noon  of  the  same  day.  She  complained  of  having  had  a  "cold" 
all  day,  pain  in  the  side  during  the  day  and  cough  only  that  afternoon. 
Blood  culture  taken  the  same  afternoon  was  negative,  but  the  sputum 
showed  a  practically  pure  culture  of  Friedlander's  pneumobacilli. 
Death  occurred  the  following  day  at  1.30  p.m.  At  autopsy  three  hours 
later,  the  right  upper  lobe  was  found  to  be  completely  consolidated, 
with  scattered  nodules  of  consolidation  in  other  lobes  of  the  lungs. 
Pure  cultures  of  Friedlander's  pneumobacillus  were  obtained  from  the 
lung,  heart's  blood,  spleen  and  liver.  In  this  case  the  symptoms  had 
lasted  only  little  longer  than  twenty-four  hours.  Weichselbaum  had 
one  case  of  primary  lobar  pneumonia  in  which  numerous  encapsulated 
pneumobacilli  were  present  in  the  sputum  and  were  found  also,  on  the 
second  day  of  the  disease,  in  pure  culture  in  the  pneumonic  exudate 
obtained  by  lung  puncture.  Death  occurred  on  the  fourth  day.  In 
one  (No.  2)  of  Apelt's2  cases,  a  blood  culture  taken  on  the  second  day 
of  the  disease  and  in  another  (No.  1)  on  the  third  day  was  positive.  In 
one  of  the  Massachusetts  General  Hospital  cases  (Autopsy  328)  death 
occurred  on  the  second  day  of  the  disease,  too  early  to  make  a  secondary 
infection  probable,  and  at  autopsy  a  pure  culture  of  this  organism  was 
obtained  from  the  lung  and  the  heart's  blood.  In  one  of  the  Rockefeller 
Hospital  cases3  (No.  1919),  a  pure  culture  of  Friedlander's  bacillus  was 
obtained  by  blood  culture  and  lung  puncture  just  before  death  on 
the  fourth  day  of  the  disease.  In  one  of  the  Massachusetts  General  Hos- 
pital cases  (Autopsy  3329),  this  organism  was  obtained  in  pure  culture 
from  the  blood  during  life  on  the  sixth  day  of  the  disease.  Death 
occurred  on  the  seventh  day.  In  addition,  the  gross  and  histologic 
character  of  the  exudate  and  the  clinical  features  and  course,  mentioned 
below,  favor  the  independence  of  this  form  of  pneumonia. 

1  I  am  indebted  to  Dr.  Henry  A.  Christian  for  the  privilege  of  using  this  case. 

2  Munch,  med.  Woch.,  April  21,  1908. 

3  I  am  indebted  to  Dr.  Rufus  Cole  for  the  privilege  of  using  his  cases.  Three  cases 
of  pneumonia  with  Friedlander's  bacilli  in  the  sputum  have  been  observed  at  the 
Hospital  of  the  Rockefeller  Institute  for  Medical  Research.  In  one  case,  Friedlander's 
bacilli  mixed  with  other  organisms  were  present  in  the  sputum  and  the  pus  obtained 
from  a  lung  abscess.  Recovery  followed  operation  by  Dr.  John  A.  Hartwell.  In  a 
second  case  a  pure  culture  was  obtained  from  the  sputum,  from  material  obtained  by 
lung  puncture  and  by  blood  culture.  Death  occurred  on  the  fourth  day.  In  the  third 
case,  Friedlander's  bacilli,  mixed  with  other  organisms,  were  found  in  the  sputum, 
but  lung  puncture  and  blood  culture  showed  pneumococci  and  no  Friedlander's  bacilli. 
This  case  illustrates  the  danger  of  reliance  on  sputum  examination  alone  for  diagnosis. 


238 


Dish'ASES  OF  THE  LUNGS 


Pathology. — Pneumonia  seen  in  connection  with  infection  with  the 
pneumobacillus  resembles  that  due  to  the  pneumococcus  in  the  lobar 
character  of  the  process  and  the  tendency  of  the  infection  to  spare  the 
pulmonary  framework,  as  indicated  by  the  absence  of  infiltration  and 
thickening  of  the' alveolar  septa.  It  differs  from  ordinary  pneumonia, 
however,  in  the  less  granular  appearance  of  the  section  surface  of  the 
lung  and  the  more  viscid  or  mucoid  exudate  poor  in  fibrin.  Softening 
of  the  pulmonary  tissue  with  abscess  formation  occurs  more  frequently 
in  this  than  in  ordinary  lobar  pneumonia.  Stuhlern1  noted  abscess 
formation  in  the  lungs  in  2  (Cases  6  and  9)  of  4  cases  of  pure  infec- 
tion with  Friedlander's  bacilli,  Apelt2  in  3  (Cases  1,  3,  and  5)  of 
7   pure   infections.      Abscess  formation  was   noted   in   none   of  the 

Fig.  37 


Friedlander's  bacillus  pneumonia.     Alveolar  exudate.      X  1000. 

6  pure  infections  at  the  Massachusetts  General  Hospital.3  Thus 
abscess  formation  has  been  noted  in  5  (27  per  cent.)  of  IS  cases.  It 
seems  probable  that  such  losses  of  pulmonary  substance  may  be 
directly  ascribed  to  the  infection  with  the  pneumobacillus.  Other 
causes  should,  however,  be  excluded.  In  one  case  (Autopsy  1488)  at 
the  Massachusetts  General  Hospital,  not  included  in  this  series,  there 
was  septicemia  due  to  Friedlander's  bacillus  and  organizing  pneu- 


1  Centralbl.  f.  Bakt.,  1904,  lte.  Abth.,  36,  p.  493.  2  Loc.  cit. 

3  Kokawa  (Deut.  Arch.  f.  klin.  Med.,  1904,  lxxx,  39)  found  a  cavity  the  size  of  a  hazel 
nut  in  one  of  nine  cases.  The  identity  of  the  organisms  in  his  cases  was  not  established 
by  culture.  Isolated  examples  of  abscess  formation  in  connection  with  pulmonary 
infection  by  Friedlander's  bacillus  have  been  reported  by  Brinckerhoff  (Med.  and 
Surg.  Rep.  Boston  City  Hosp.,  1901,  S.  12),  and  Lenhartz  (Nothnagel's  Spec.  Path. 
u.  Ther.,  1904,  III,  Bd.  ii,  301). 


FRIEDL AN DEE'S  BACILLUS  PNEUMONIA  239 

monia  with  abscess  formation  involving  parts  of  both  lungs.  J.  II. 
Wright  found  actinomyces  as  a  probable  cause  of  the  destructive 
pulmonary  process.  Anaerobic  cultures  should  be  made  in  these 
cases. 

On  histologic  examination,  the  alveoli  are  found  to  contain  an 
exudate  of  serum,  red-blood  corpuscles,  pus  cells  and  fibrin.  The  red- 
blood  corpuscles  are  perhaps  less  numerous  than  in  ordinary  lobar 
pneumonia.  The  fibrin  is  less  abundant.  A  striking  feature  of  the 
exudate  is  the  presence  of  varying  and  at  times  considerable  numbers 
of  large  cells  with  a  single,  oval  or  round  nucleus  and  vacuolated  pro- 
toplasm. These  cells  are  phagocytic  for  pigment,  red-blood  corpuscles, 
pus  cells  and  the  bacilli.  In  some  parts  of  the  sections  these  cells 
comprise  a  large  part  of  the  exudate.  They  are  probably  desquamated 
epithelial  cells.  Enormous  numbers  of  encapsulated  bacilli  may  be 
present  in  the  exudate,  both  within  and  without  the  cells. 

Symptoms. — In  their  symptoms  of  onset  and  course  the  cases  present 
no  distinctive  clinical  features.  Herpes  appears  to  be  less  frequent 
than  in  ordinary  lobar  pneumonia.  An  initial  chill  is  usually  absent. 
The  onset  is  commonly  acute  with  pain  in  the  side,  cough  and  dyspnea. 
Delirium  is  often  observed.  The  sputum  is  blood-streaked,  or  rusty, 
or  consists  of  almost  pure  blood.  Its  mucoid  character  is  striking  in 
some  cases.  Smear  preparations  of  the  sputum  may  show  enormous 
numbers  of  Friedlander's  bacilli  and  only  few  cells.  The  white  count 
at  entrance  numbered  3400,  5000,  10,000  and  11,000  in  four  of  the 
Massachusetts  General  Hospital  cases,  28,000  in  the  case  at  the  Peter 
Bent  Brigham  Hospital.  In  Brinckerhoff's1  case  it  was  33,800.  In 
the  Rockefeller  Hospital  case  (No.  1919)  it  was  21,900.  As  all  these 
cases  proved  fatal,  the  white  count  cannot  be  regarded  as  having  an 
important  prognostic  significance.  The  temperature  is  remittent  or 
continuous.  In  general  it  may  be  said  that  the  course  of  the  disease 
is  more  severe  than  that  of  ordinary  lobar  pneumonia.  A  fatal  ter- 
mination may  occur  on  the  second  or  third  day  of  the  disease,  which 
is  unusual  in  ordinary  pneumonia. 

Complications. — Fibrinous  pleuritis  is  constantly  present.  A  sero- 
fibrinous or  purulent  effusion  may  be  added.  Meningitis,  pericarditis, 
or  endocarditis  may  occur  as  complications.  The  frequency  of  pul- 
monary abscess  has  already  been  mentioned.  Septicemia  occurred 
in  all  the  Massachusetts  General  Hospital  cases. 

Diagnosis. — This  cannot  be  made  with  certainty  from  examination 
of  the  sputum  alone.  Friedlander's  bacilli  may  predominate  in  the 
sputum  and  yet  the  pulmonary  process  may  be  due  to  another  cause. 
A  pure  culture  of  the  organism  obtained  from  material  secured  by 
lung  puncture  is  the  most  conclusive  clinical  evidence  of  Friedlander's 
bacillus  pneumonia.  Positive  blood  cultures  indicate  a  general 
infection. 

1  Loc.  cit. 


240  DISEASES  OF  THE  LUNGS 

Prognosis.— The  mortality  is  very  high.  No  well-established 
instance  of  lobar  pneumonia  due  to  pure  infection  with  Friedlander's 
bacillus  is  known  to  have  recovered. 

Treatment. — This  is  the  same  as  for  ordinary  lobar  pneumonia. 
Pulmonary  abscess  complicating  Friedlander's  bacillus  pneumonia 
should  be  treated  on  the  principles  outlined  in  the  section  on  Abscess 
and  Gangrene. 


CHAPTER  XII. 
PSITTACOSIS. 

Psittacosis  (from  (phxaxoc,  parrot)  is  a  term  applied1  to  severe 
acute  infections  occurring  for  the  most  part  as  house  epidemics  and 
thought  to  be  due  to  transmission  from  diseased  parrots  to  man.  In 
parrots  the  disease  is  characterized  by  the  occurrence  of  chronic  enter- 
itis with  diarrhea  and  foul  odor  to  the  fecal  material.  The  birds  become 
apathetic  and  somnolent,  the  wings  droop,  the  appetite  is  lost  and  death 
occurs  with  convulsions.  Pneumonia  is  not  observed.  In  man  the 
disease  has  been  characterized  as  a  severe  typhoidal  condition  Math 
atypical  pneumonia.  No  conclusive  evidence  of  transmission  from 
parrots  to  man  has  yet  been  produced.  Bacteriologic  studies  have 
not  served  to  establish  any  direct  relation  between  diseased  birds  and 
infection  in  man,  and  the  independence  of  this  disease  is  doubtful. 
Leichtenstern2  critically  reviewed  the  literature. 

Bacteriology. — Eberth3  in  1880  found  micrococci  in  the  internal 
organs  of  a  gray  parrot.  Wolff4  in  1883  investigated  12  parrots  for  the 
purpose  of  explaining  the  high  mortality  among  the  birds  imported 
into  Europe  in  large  numbers  from  the  West  Coast  of  Africa.  Micro- 
cocci were  found  in  almost  all  the  organs.  Nocard5  in  1893  constantly 
succeeded  in  isolating  a  bacillus  from  the  bone-marrow  of  parrots 
which  had  died  on  the  way  from  Buenos-Ayres  to  Havre.  This 
organism  he  described  as  a  short,  rather  thick,  motile  bacillus,  with 
rounded  ends.  Growth  took  place  on  all  the  usual  solid  and  fluid  media 
of  a  neutral  or  slightly  alkaline  reaction  under  aerobic  and  anaerobic 
conditions;  lactose  was  not  fermented,  milk  was  not  coagulated,  and 
gelatin  was  not  liquefied.  The  bacillus  decolorized  by  Gram's  method 
of  staining.  Feeding  experiments  and  subcutaneous  inoculation  of 
parrots,  pigeons,  hens,  mice,  rabbits  and  guinea-pigs  caused  death 
from  "hemorrhagic  septicemia."  Pure  cultures  of  the  organism  could 
be  recultivated  from  all  the  organs.  Three  years  later  Gilbert  and 
Fournier6  found  a  bacillus  similar  to  that  described  by  Nocard,  in 
the  heart's  blood,  the  spleen,  and  the  bone  marrow  in  one  parrot  dying- 
after  several  days  of  abundant  diarrhea. 

1  Morange  (De  la  psittacose  ou  infection  speciale  determinee  par  les  perruches, 
These  de  Paris,  1895) . 

2  Centralbl.  f.  allg.  Gesundheitspflege,  1899,  xviii,  241. 

3  Virchow's  Arch.,  1880,  Bd.  lxxx,  p.  311.  4  Ibid.,  1883,  Bd.  xcii,  p.  252. 

5  Conseil  d'hygiene  publ.  de  la  Seine,  24  mars,  1892,  Annexe,  B.,  p.  14. 

6  Sur  un  memoire  de  MM.  les  Drs.  Gilbert  et  Fournier  (Contribution  a  l'etude  de  la 
psittacose)  au  nom  d'une  Commission  composee  de  MM.  Nocard  et  Debove,  rapporteur, 
Bull,  de  l'Acad.  de  Med.,  1896,  3  S.,  35-36,  429. 

16 


242  DISEASES  OF    THE  LUNGS 

In  one  instance  Gilbert  and  Fonrnier  demonstrated  Nocard's  bacillus 
in  the  heart's  blood  at  autopsy  in  one  of  Mathieu's1  patients  with 
psittacosis.  Examination  of  the  sputum,  pleural  fluid  and  blood 
obtained  By  puncture  of  the  spleen,  three  days  before  death,  had 
previously  been  negative.  According  to  their  observations,  Nocard's 
bacillus  resembled  the  colon  and  typhoid  bacillus,  but  differed  from 
the  latter  in  the  appearance  of  the  growth  on  potato  and  gelatin  and 
its  extreme  virulence  for  laboratory  animals.  The  organism  was 
agglutinated,  but  without  loss  of  motility,  by  the  serum  of  a  patient 
with  typhoid  in  a  dilution  of  1  to  10.  Xicolle2  found  that  in  one  case 
the  blood  serum  of  a  patient  with  psittacosis  agglutinated  Nocard's 
bacillus  in  dilutions  of  1  to  50  and  1  to  60.  This  same  serum  was  active 
against  the  typhoid  bacillus  at  1  to  30,  but  inactive  against  the  colon 
bacillus.  In  a  second  case  the  blood  serum  agglutinated  Nocard's 
bacillus  on  one  occasion  in  a  dilution  of  1  to  10,  but  was  inactive 
against  the  other  organisms.  In  a  third  case,  the  serum  produced  no 
agglutination  with  the  three  organisms.  Others3  have  failed  to  con- 
firm Nocard's  and  Gilbert  and  Founder's  findings. 

Investigation  by  Netter  of  the  pneumonic  exudate  from  patients 
with  the  disease  showed  the  diplococcus  pneumonia?.  Rendu  and  Tri- 
boulet  found  the  diplococcus  pneumonia?  and  staphylococci  in  the 
pneumonic  sputum.  Halle  found  colon  bacilli  in  the  sputum  of  one 
patient  and  diplococcus  pneumonia?  in  another  by  mouse  inoculation. 
Weinberg  demonstrated  diplococcus  pneumonia?  and  staphylococcus 
in  the  sputum  (quoted  from  Leichtenstern.).  Czaplewski  investigated 
Leichtenstern's  fatal  case,  finding  streptococcus  mixed  with  other 
organisms  in  the  lung.  He  came  to  the  conclusion  that  the  parrot 
did  not  die  from  infection  with  Nocard's  psittacosis  bacillus,  and  that 
no  conceivable  etiologic  connection  could  be  recognized  between  the 
disease  of  the  parrot  and  the  illness  of  those  in  the  house.  He  adds 
however,  that  the  possibility  of  an  infectious  disease  of  parrots  trans- 
missible to  man  cannot  be  denied. 

Epidemics. — Small  outbreaks  affecting  several  members  of  a  house- 
hold and  ascribed  to  contagion  from  parrots  were  reported  by  Ritter,4 
Ost,5  and  Wagner.6  In  Paris,  during  the  year  1892,  following  a  large 
importation  of  parrots  from  Buenos-Ayres,  there  wTere  49  cases  with 
16  deaths.  In  1893,  there  were  7  cases  with  5  deaths;  in  1894,  2  cases 
both  of  which  recovered;  and  from  1895  to  1896,  12  cases  with  3  deaths. 
In  the  winter  of  1894  and  1895,  house  epidemics,  described  by  Banti 

i  Gaz.  des  Hop.,  1896,  13  ct  15  aout. 

2  Serodiagnostic  de  la  psittacose,  Mem.  de  la  Soc.  de  Biol.,  1898,  p.  1171. 

3  Achard  and  Bensaude  (Presse  med.,  25  Nov.,  1896,  p.  639)  found  an  organism 
identical  with  Nocard's  bacillus  in  the  urine  from  a  patient  with  a  condition  suggesting 
typhoid,  and  in  another  case  in  the  purulent  contents  of  an  inflammation  of  the  right 
sternoclavicular  joint. 

■>  Correspondenz-Blatt  f.  Schw.  Aerzte.,  1879,  9,  p.  570. 

5  [bid.,  1883,  p.  424. 

«  Deut.  Arch.  f.  klin.  Med.,  1884,  xxxv,  191,  and  ibid.,  1888,  xlii,  411. 


PSITTACOSIS  243 

and  Malenchini  and  by  Palamidessi,1  occurred  in  Florence  and  Ponto. 
In  1896,  Haedke2  observed  a  house  epidemic  in  Stettin.  In  1897,3  cases 
were  reported  in  Genoa,  and  in  18984  in  Bernay  in  the  North  of  France. 
Leichtenstern  observed  house  epidemics  in  Cologne  during  1898.  In 
one  epidemic  there  were  10  cases  with  4  deaths,  and  in  a  second  8 
cases  with  1  death.  In  1904,  Vickery  and  Richardson5  reported  3  cases 
of  probable  psittacosis  with  recovery. 

The  usual  experience  has  been  that  several  members  of  a  household 
in  close  contact  with  a  sick  parrot  have  been  taken  ill  almost  simul- 
taneously, the  explosive  character  of  the  outbreak  thus  suggesting 
contagion  from  a  common  source  rather  than  from  person  to  person. 
The  occurrence  of  outbreaks  in  numerous  houses  to  which  parrots 
had  been  delivered  in  different  parts  of  Paris  during  the  epidemic 
of  1892  lends  support  to  the  view  that  the  infection  was  transmitted 
from  them  to  man.  The  infrequency  of  the  disease  compared  with  the 
innumerable  opportunities  for  contagion  among  ship's  crews,  bird 
handlers  and  lovers  of  pets  is  against  it. 

Pathology. — The  number  of  cases  in  which  postmortem  findings 
are  reported  is  too  small  to  permit  of  a  conclusion  concerning  the  type 
of  the  pneumonic  process.  In  Ritter's6  3  cases,  the  condition  was 
described  as  "lobular,  serous-croupous  pneumonia."  Gastou7  found 
total  lobar  pneumonic  infiltration.  The  cut  surface  was  of  firm  con- 
sistency, dark  bluish  red,  moist  and  smooth.  In  Leichtenstern' s  case 
the  pneumonia  was  cellular  and  fibrinous. 

Symptoms. — The  incubation  period  appears  to  be  from  one  to  three 
weeks.  The  onset  is  usually  acute,  at  times  insidious.  A  chill  or  chilli- 
ness commonly  initiates  the  attack.  The  temperature  is  quickly 
elevated  and  continuous  or  remittent,  lasting  from  eight  days  to  three 
weeks.  Defervescence  is  usually  by  lysis,  at  times  by  crisis.  At 
onset  there  is  severe  prostration.  Headache  is  constant.  The  appetite 
is  lost.  Vomiting  is  seldom  observed.  Constipation  is  more  common 
than  diarrhea,  in  contrast  to  the  disease  in  parrots.  Cough  is  present 
from  the  outset.  Delirium,  apathy,  and  stupor  were  frequent  among 
the  Paris  cases.  Dyspnea,  pain  in  the  side,  and  cyanosis  are  likely 
to  occur  with  pneumonia,  the  development  of  which  is  usually  insidious, 
but  may  be  acute,  as  in  typical  croupous  pneumonia.  The  sputum 
may  be  absent,  mucoid  or  rusty.  On  examination  there  are  signs 
suggestive  of  lobular  or  lobar  pneumonia.  In  some  cases  evidences 
of  consolidation  may  be  lacking.  Herpes  is  absent.  In  rare  instances 
a  roseola-like  eruption  and  petechial  spots  have  been  noted.  The 
spleen  is  usually  enlarged.  In  Leichtenstern's  cases,  delirium  was 
usually  absent,  diarrhea  was  noted  in  several  cases  and  the  spleen  was 
not  found  to  be  enlarged.    Convalescence  was  protracted. 

1  Leichtenstern,  loc.  cit.  2  Deut.  med.  Woch.,    1S9S,  xiv. 

3  Lancet,  1897,  p.  1058.  4  Leichtenstern,  loc.  cit.,  p.  271. 

6  Trans.  Assoc.  Amer.  Phys.,  1904,  xix,  364.  6  Loc.  cit. 

7  Quoted  from  Leichtenstern,  loc.  cit.,  p.  264. 


244  DISEASES  OF  THE  LUNGS 

Diagnosis. — Aside  from  the  occurrence  of  atypical  pneumonia 
from  apparent  contact  with  diseased  parrots,  there  are  no  distinctive 
features.  The  clinical  aspects  and  course  are  similar  to  those  seen  in 
bronchopneumonia  and  atypical  lobar  pneumonia  at  times  observed 
without  relation  to  possible  infection  from  birds. 

Prognosis. — Among  91  reported  cases  there  were  29  deaths,  a  mor- 
tality of  31.8  per  cent.  The  pneumonia  appears  to  be  principally 
concerned  in  the  fatal  termination. 

Prophylaxis. — The  connection  between  disease  in  parrots  and  man 
can  neither  be  affirmed  nor  denied.  Intimate  contact  with  diseased 
parrots  must,  however,  be  regarded  as  highly  undesirable  and  is  to 
be  avoided  by  preventing  their  sale  and  their  removal  from  the  house, 
if  they  become  ill  after  purchase.  In  addition,  it  is  desirable  that 
recently  imported  parrots  be  held  in  quarantine  before  they  are  offered 
for  sale. 

Treatment. — This  is  that  of  ordinary  pneumonia. 


CHAPTER  XIII. 
BRONCHOPNEUMONIA. 

In  this  form  there  is  an  inflammation  of  the  bronchi,  the  terminal 
bronchioles  and  the  adjacent  or  the  terminal  air  vesicles,  hence  the 
term  bronchopneumonia ,  Because  of  its  almost  constant  origin  in 
bronchial  catarrh,  it  is  also  called  catarrhal  pneumonia.  Involve- 
ment of  the  lobules  rather  than  the  entire  lobe,  justifies  the  term 
lobular  in  contradistinction  to  lobar  pneumonia.  Inasmuch  as  capil- 
lary bronchitis  is  invariably  associated  with  inflammatory  changes  in 
the  lung,  it  cannot  be  regarded  as  having  an  independent  existence, 
and  is  included  among  cases  classed  as  bronchopneumonia.  Tuber- 
culous bronchopneumonia  represents  an  important  group. 

Historical  Note. — Bronchopneumonia  was  not  sharply  differentiated 
from  other  affections  and  given  an  independent  place  by  the  older 
writers.  The  failure  to  describe  it  as  an  important  complication  of 
measles  indicates,  as  Jurgensen1  suggests,  that  it  was  not  well  under- 
stood. Even  Laennec2  did  not  definitely  separate  bronchopneumonia 
from  other  affections,  but  refers  to  small,  scattered  areas  of  pneumonic 
infiltration  complicating  "suffocative  catarrh,"  and  cites  as  an  example 
a  case  of  Andral's.3  Barthez  and  Rilliet4  were  the  first  definitely  to 
separate  catarrhal  from  croupous  pneumonia.  Bartels'5  description 
of  the  gross  pathologic  findings  and  clinical  features  of  catarrhal 
pneumonia  complicating  measles  was  an  important  contribution. 

Frequency. — This  varies  with  the  age  of  the  patients.  In  infancy 
and  up  to  about  two  years  of  age  a  great  majority  of  the  cases  of 
primary  pneumonia  are  of  this  type.  Thus,  of  322  cases  of  primary 
pneumonia  observed  by  Holt6  during  the  first  two  years  of  life,  there 
were  242  (75  per  cent.)  of  bronchopneumonia  and  80  (25  per  cent.) 
of  lobar  pneumonia.  In  later  childhood  and  in  adult  life  the  fre- 
quency of  bronchopneumonia  diminishes,  while  that  of  lobar  pneu- 
monia increases.  Of  2459  cases  of  pneumonia  at  the  Massachusetts 
General  Hospital,  where  children  form  only  a  small  proportion  of 
the  total  admissions,  the  clinical  diagnosis  of  bronchopneumonia 
was  made  339  times  (13  per  cent.)  during  the  seventeen  years  from 
1897  to   1914,  while  the  cases   of  lobar  pneumonia   number  2120 

1  Handb.  d.  spec.  Path.  u.  Ther.  Ziemssen.,  1874,  v,  184. 

2  Traite  de  l'auscultation  med.,  T.  i. 

3  Clin,  med.,  T.  ii,  observ.  46. 

4  Traite  clinique  et  pratique  des  maladies  des  enfants,  Paris,  Baillieres,  1853,  2d  ed. 
6  Virchow's  Arch.,  1861,  Bd.  xxi,  p.  65. 

6  Diseases  of  Infancy  and  Childhood,  1903,  2d  ed.,  p.  525. 


246  DISEASES  OF  THE  LUNGS 

(86  per  cent.)  during  the  same  period.  During  both  childhood  and 
adult  life  nearly  all  the  cases  of  secondary  pneumonia  arc  of  this 
type,  and  the  disease  is  actually  much  more  frequent  than  figures 
based  on  clinical  statistics  alone  seem  to  show.  Among  3000  autopsies 
at  the  Massachusetts  General  Hospital  the  number  of  cases  showing 
bronchopneumonia  outnumber  those  with  lobar  pneumonia,  there 
being  273  of  the  former  and  211  of  the  latter. 

Etiology. — The  two  sexes  are  about  equally  affected.  As  with 
lobar  pneumonia,  cases  of  bronchopneumonia  are  more  frequent 
during  the  colder  months  of  the  year.  The  previous  condition  of  the 
patients  is  a  variable  factor,  but  it  may  in  general  be  said  that  the 
disease  is  more  common  among  the  poorer  classes,  in  patients  who 
are  undernourished  and  where  there  is  overcrowding  and  bad  venti- 
lation. Premature  infants,  the  inmates  of  infant  asylums,  and  the 
subjects  of  rickets,  syphilis,  or  infantile  diarrhea  are  not  infrequently 
attacked. 

The  influence  of  exposure  is  difficult  to  estimate,  and  while  it  cannot 
be  regarded  as  a  cause  of  the  disease,  yet  in  patients  with  an  existing 
respiratory  infection,  it  seems  probable  that  sudden  chilling  of  the 
surface  of  the  body  may  be  a  contributing  factor  in  aggravating  the 
infection  and  leading  to  invasion  of  the  lung. 

Primary  acute  bronchopneumonia  is  essentially  a  disease  of  child- 
hood and  the  first  three  years  of  life,  and  may  attack  children  in 
previous  good  health  or  debilitated  subjects.  Of  443  cases  of  broncho- 
pneumonia observed  by  Holt  in  infants  and  young  children,  164  were 
primary.  After  the  age  of  four,  primary  bronchopneumonia  must  be 
very  uncommon.  Of  195  cases  of  bronchopneumonia  which  have  come 
to  autopsy  at  the  Massachusetts  General  Hospital,1  only  14  represent 
the  primary  form  of  the  disease,  and  all  were  four  years  of  age  or  under. 
I  have  never  seen  a  case  in  which  a  healthy  adult  has  been  stricken 
with  pneumonia  unpreceded  by  bronchitis  in  which  at  autopsy  the 
condition  was  proved  to  be  uncomplicated  bronchopneumonia. 

Secondary  bronchopneumonia  occurs  more  frequently  during  child- 
hood than  in  adult  life,  but  is  met  at  all  ages,  and  is  not  infrequent 
in  the  aged.  The  conditions  to  which  the  bronchopneumonia  is 
secondary  may  be  divided  into  three  groups. 

1.  Cases  Complicating  or  folloiving  the  Acute  Infections. — In  child- 
hood, measles,  whooping  cough,  and  diphtheria  are  responsible  for  the 
largest  number  of  cases,  and  a  considerable  proportion  of  the  deaths 
in  these  diseases  is  due  to  bronchopneumonia.  Infection  of  the  lungs 
secondary  to  bronchitis  of  the  larger  tubes  is  also  a  common  method 
of  origin.  Bronchopneumonia  also  occurs  as  a  complication  of  infantile 
diarrhea,  scarlet  fever,  smallpox,  erysipelas,  and  varicella. 

In  adults,  the  disease  is  most  commonly  secondary  to  a  pre- 
existing infection  of  the  air  passages  and  is  not  infrequent  in  the  more 

1  Where  children  comprise  only  a  small  proportion  of  the  total  admissions. 


BRONCHOPNEUMONIA  247 

severe  types  of  acute  bronchitis.  It  also  occurs  as  a  recurrent  infec- 
tion in  bronchiectasis,  chronic  interstitial  pneumonia  and  pulmonary 
abscess.  Empyema  breaking  through  into  the  lung  may  also  be  a 
cause.  Lobar  and  bronchopneumonia  at  times  coexist  as  found  at 
autopsy  in  six  of  the  present  series.  Bronchopneumonia  may  com- 
plicate pulmonary  tuberculosis. 

Abdominal  suppuration  is  frequently  complicated  by  broncho- 
pneumonia which  may  arise  by  direct  extension  or  by  metastasis. 
In  fatal  cases  in  adults,  peritonitis  occupies  a  prominent  place  as  a 
cause  and  was  found  in  35  out  of  195  cases.  The  source  of  the  peri- 
tonitis is  probably  of  little  moment,  and  may  be  local  or  general. 
Bronchopneumonia  may  arise  in  the  course  of  all  forms  of  meningitis, 
in  endocarditis,  pericarditis,  otitis  media,  endometritis,  metritis, 
salpingitis,  parotitis,  infections  of  the  urinary  tract,  and  other  infec- 
tions.   It  occurs  in  typhoid  and  usually  as  a  terminal  event. 

Obstruction  of  the  bronchi  by  pressure  from  without  of  malignant 
growth  or  aneurysm  may  lead  to  the  retention  of  bronchial  secretion, 
secondary  infection  and  purulent  bronchitis,  bronchiectasis,  and 
bronchopneumonia.  Partial  occlusion  of  a  bronchus  by  a  new  growth 
springing  from  the  bronchial  wall  may  lead  to  similar  changes.  In 
one  of  the  present  series  (Autopsy  2503),  a  small  adenocarcinoma 
of  the  left  primary  bronchus  gave  rise  to  bronchiectasis  and  chronic 
inflammatory  changes  with  abscess  formation  in  the  left  lung  and 
acute  bronchopneumonia  of  the  right  lower  lobe. 

2.  Cases  Occurring  in  Debilitating  Conditions. — Debilitating  condi- 
tions of  various  sorts  are  often  complicated  by  bronchopneumonia, 
especially  as  a  terminal  infection.  The  later  stages  of  malignant 
disease,  broken  cardiac  compensation,  chronic  nephritis,  cerebral 
hemorrhage,  brain  tumors,  pernicious  and  severe  secondary  anemia, 
leucemia,  exophthalmic  goitre,  diabetes,  and  other  diseases  may  be 
thus  complicated. 

3.  Aspiration  Pneumonia. — The  experiments  of  Traube1  showed 
that  the  pulmonary  changes  following  section  of  both  vagus  nerves 
were  due  to  the  entrance  of  buccal  secretion  into  the  air  passages. 
The  consequent  insensibility  of  the  larynx  results  in  the  inhalation  of 
food,  drink  or  septic  material  into  the  lungs,  and  an  intense  and  even 
gangrenous  bronchopneumonia.  Such  an  aspiration  or  deglutition 
pneumonia  may  occur  when  the  larynx  is  insensitive,  as  in  intoxication 
with  alcohol,  ether,  or  chloroform,  in  the  stupor  or  unconsciousness 
of  apoplexy,  uremia,  meningitis,  cerebral  hemorrhage  or  submersion. 
The  danger  is  increased  when  there  is  already  an  infection  of  the 
respiratory  tract,  when  vomiting  occurs  in  a  semiconscious  patient, 
or  when  following  an  abdominal  operation  there  is  a  suppression 
of  expulsive  efforts  to  free  the  air  passages  of  foreign  particles.  This 
form   of  pneumonia  is  not  uncommon  following   operations   about 

1  Ges.  Beitr.  z.  Path.  u.  Physiol.,  1846,  Bd.  i. 


24S  DISEASES  OF  THE  LUNGS 

the  nose  or  mouth,  the  removal  of  adenoids,  with  cancer  of  the  larynx 
or  esophagus,  and  after  intubation  or  tracheotomy.  The  aspira- 
tion of  a  foreign  body  into  the  lung  is  almost  invariably  followed  by 
bronchopneumonia  unless  the  body  is  at  once  removed. 

Bronchopneumonia  may  follow  the  aspiration  into  near-by  or 
remote  parts  of  the  lung  of  pus  from  a  bronchiectatic  cavity,  a  focus 
of  abscess  or  gangrene  or  an  empyema  rupturing  into  the  lung.  A 
tuberculous  bronchopneumonia  may  follow  the  inhalation  of  blood 
during  hemoptysis. 

Bacteriology. — One  organism  was  found  as  the  apparent  sole  cause 
of  the  primary  or  secondary  bronchopneumonia  in  infants  or  adults, 
usually  in  more  than  one-half  of  the  cases,  by  Weichselbaum,1 
Karlinski,2  Neumann,3  Queisner,4  Netter,5  Wright  and  Stokes,6 
Kreibich,7  Diirck,8  Wollstein,9  and  others.  The  pneumococcus  and 
streptococcus  were  the  most  common  single  invaders  and  a  smaller 
number  of  cases  showed  the  staphylococci  and  Friedlander's  bacillus. 
The  influenza  bacillus  may  readily  be  overlooked  unless  carefully 
sought.  The  micrococcus  catarrhalis  has  received  little  attention, 
but  is  apparently  also  the  occasional  sole  cause  of  bronchopneumonia 
as  in  the  cases  reported  by  Ghon,  Pfeiffer  and  Sederl.10  When  these 
organisms  are  taken  into  account,  it  seems  to  be  true  of  bronchopneu- 
monia, both  in  infancy  and  adult  life,  whether  primary  or  secondary, 
that  mixed  infections  are  the  rule,  and  that  to  no  one  infecting  agent 
can  the  disease  be  especially  ascribed.  Pure  cultures,  even  when  the 
sputum  is  collected  with  great  care,  are  relatively  uncommon,  and 
although  now  one  and  then  another  organism  may  predominate  in 
single  specimens,  yet  in  the  presence  of  a  mixed  infection,  the  observer 
must  remain  in  doubt  as  to  the  relative  importance  of  any  one  group 
of  bacteria.  The  diphtheria  bacillus  is  to  be  reckoned  with  in  the 
bronchopneumonia  secondary  to  diphtheria,  and  was  found  in  52 
of  128  cases  of  bronchopneumonia  by  Pearce.11  It  was  unassociated 
with  other  organisms  in  17  cases.  Pulmonary  infection  with  diphtheria 
bacilli  may  also  be  primary.  Persistent  infection  of  the  lung  with 
diphtheria  bacilli  may  occur.  Petruschky12  found  diphtheria  bacilli 
in  the  expectoration  of  one  patient  three  years  after  diphtheria. 
Physical  examination  was  negative.  In  Schmidt's13  case  in  which  the 
original  infection  probably  occurred  ten  years  previously,  organisms 
morphologically  and  culturally  like  diphtheria  bacilli  were  present 
in  the  mucopurulent  sputum  in  pure  culture.     Examination  of  the 

I  Wiener,  med.  Jahrb.,  1886,  Ixxxii,  483.  2  Fort.  d.  Med.,  1889,  vii,  681. 
3  Jahrb.  f.  Kinderh.,  1889-90,  xxx,  233.  4  Ibid.,  p.  277. 

*  Arch,  de  med.  exp.,  1892,  iv,  28. 

6  Boston  Med.  and  Surg.  Jour.,  1895,  No.  14,  vol.  cxxxii. 

7  Beitrage  z.  klin.  Med.  u.  Chir.,  1896,  H.  13. 

8  Deut.  Arch.  f.  klin.  Med.,  1897,  vol.  lviii. 

9  Jour.  Exp.  Med.,  1901-05,  vol.  vi.  10  Zeit.  f.  klin.  Med.,  1902,  vol.  xliv. 

II  Boston  Med.  and  Surg.  Jour.,  December  2,  1897. 

12  "Gesundheit,"  1912,  Nos.  1  and  2. 

13  Munch,  med.  Wroch.,  January  7,  1913. 


BRONCHOPNEUMONIA  249 

lungs  suggested  chronic  interstitial  pneumonia.  The  organisms  were 
avirulent.    Infection  with  pest  bacilli  also  occurs. 

Thus  far  the  attempt  to  correlate  the  clinical  picture  with  the 
cultural  findings  has  failed,  and  in  their  symptoms  of  onset,  clinical 
course  and  termination,  there  seems  to  be  no  striking  or  constant 
difference  in  the  various  single  or  multiple  groups  of  infection. 

A  general  infection  is  present  in  a  majority  of  the  terminal  broncho- 
pneumonias. 

Experimental  Bronchopneumonia. — Wollstein  and  Meltzer1  find  that 
intrabronchial  insufflation  of  dogs  with  pure  cultures  of  the  strepto- 
coccus or  of  the  influenza  bacillus  produces  bronchopneumonia  and 
not  lobar  pneumonia.  Pneumococci  produce  lobar  pneumonia,  as 
shown  by  Lamar  and  Meltzer,2  and  Wollstein  and  Meltzer.3 

Pathogenesis. — Atelectasis  was  regarded  by  Bartels  as  an  important 
feature  of  the  origin  of  bronchopneumonia,  but  it  is  difficult  to  under- 
stand how  it  can  play  any  essential  part  in  the  production  of  the  dis- 
ease, and  it  seems  to  be  regarded  rather  as  a  consequence  than  as  a 
cause.  Its  frequent  occurrence  may  be  ascribed  to  occlusion  of  the 
bronchial  lumen  by  swelling  of  the  mucosa.  The  air  imprisoned  in 
the  involved  region  is  then  partly  absorbed  and  partly  expelled  by 
succeeding  expirations  with  or  without  the  favoring  influence  of 
expulsive  efforts  with  cough,  while  its  renewal  is  prevented  by  the 
bronchial  obstruction  and  the  deficient  force  of  inspiration.  The 
essential  factor  in  the  disease,  irrespective  of  the  occurrence  of  atelec- 
tasis, seems  to  be  the  direct  extension  of  an  infective  agent  downward, 
along  or  through  the  walls  of  the  bronchi.  Collapse  of  the  alveoli 
may  precede  or  accompany  the  process,  or  it  may  be  absent. 

Pathology. — Gross  Appearance. — Atelectasis  is  a  frequent  fore- 
runner or  accompaniment  of  bronchopneumonia  in  infants.  In  the 
early  stages  of  the  disease,  the  posterior  inferior  margins  of  the  lungs 
are  involved,  and  later  the  anterior  and  upper  marginal  portions  as 
well.  In  some  cases  an  airless  strip  of  lung  tissue  from  1  to  2  inches 
wide  is  found  to  extend  from  the  base  toward  the  apex  on  the  pos- 
terior aspect  of  the  lung,  and  bounded  both  toward  the  spine  and 
the  axilla  by  air-holding  tissue.  In  rare  instances,  a  considerable  part 
or  even  the  whole  of  one  lobe  or  one  lung  may  be  atelectatic. 
Collapsed  areas  are  bluish,  dark  blue,  blue  black  or  violet  in  sharp 
contrast  to  the  pale  red  of  the  neighboring  and  uninvolved  parts,  of 
diminished  volume,  and  hence  depressed  below  the  level  of  the 
neighboring  pulmonary  surface,  firm  to  the  touch,  and  on  section, 
are  found  to  contain  only  a  small  amount  of  dark  blood.  Crepitation 
is  absent.  If  the  collapse  is  recent  and  still  uninflamed,  it  is  capable 
of  reinflation  by  means  of  a  blow  pipe  inserted  into  the  bronchus, 
and  then  resumes  the  normal  pale  red  color  and  former  volume.    But 

1  Jour.  Exp.  Med.,  1912,  xvi,  126. 

2  Ibid.,  1912,  xv,  133. 

*  Ibid.,  1913,  xvii,  353. 


250  DISEASES  OF  THE  LUNGS 

if  already  the  site  of  bronchopneumonia  infiltration,  it  is  at  first 
only  partially  and  later  not  at  all  reinflatable. 

Bronchopneumonia  areas  an;  usually  bilateral,  often  symmetrically 
placed  and  commonly  involve  the  lower  lobes,  although  they  may 
be  found  at  any  place  in  the  lung.  Of  85  cases  studied  at  the  Massa- 
chusetts General  Hospital,1  the  lower  lobes  were  predominantly 
affected,  the  left  lobe  being  involved  45  and  the  right  54  times.  In 
the  superior  lobes,  the  process  was  found  on  the  right  side  in  30  cases 
and  on  the  left  in  24.  The  middle  lobe  of  the  right  lung  showed  the 
smallest  number  of  infections  being  involved  in  14  instances. 

Infiltration  of  an  atelectatic  region  may  be  indicated  by  a  dark 
red  color,  the  presence  of  a  dark  red  serum  and  greater  difficulty  in 
reinflation.  Patches  of  bronchopneumonia  may  appear  within  the 
collapsed  tissue  or  in  parts  of  the  lung  not  so  involved,  and  atelectasis 
is  not  a  necessary  feature  of  the  process.  The  bronchopneumonic 
patches  can  be  felt  as  hard,  solid,  round  or  nodular  areas  within  the 
tissue.  Crepitation  is  absent.  They  are  usually  multiple,  and  when 
discrete,  vary  in  size  from  that  of  a  pin's  head  to  a  pigeon's  egg  or 
larger,  and  are  at  first  reddish  brown  and  firm,  later,  grayish  red  or 
pale  gray  and  friable.  Over  peripheral  areas,  the  pleura  may  be 
slightly  turbid  and  granular  and  show  minute  hemorrhages.  On 
section,  the  bronchopneumonic  patches  project  slightly  above  the 
level  of  the  neighboring  lung,  are  more  or  less  sharply  circumscribed 
about  a  central  bronchus  from  which  a  small  amount  of  tenacious 
purulent  fluid  can  be  expressed,  and  present  a  smooth  non-granular 
surface.  The  section  surface  exudes  a  white  or  gray  purulent  fluid 
on  pressure.  When  the  ramifications  of  the  bronchi  are  cut  and 
followed  into  the  involved  territory,  the  patches  of  bronchopneumonia 
are  found  to  be  lateral  or  terminal  in  respect  to  their  relation  to  the 
bronchial  divisions.  Early  in  their  development,  scattered  areas  of 
bronchopneumonia  may  appear  as  minute  grayish-yellow,  tubercle- 
like  granulations  when  seen  through  the  pleura.  Isolated  larger 
areas  are  separated  by  uninflamed  tissue,  but  confluent  broncho- 
pneumonia may  lead  to  tolerably  compact,  homogeneous  infiltration, 
resembling  lobar  hepatization.  The  infiltration  is,  however,  less 
uniform  than  in  croupous  pneumonia,  dark  bands  of  collapsed  tissue 
or  strips  of  air-holding  and  crepitant  alveoli  may  intervene  between 
the  infiltrated  areas,  the  section  surface  is  smooth  rather  than 
granular,  fibrin  is  scanty  or  absent,  and  on  microscopic  examination 
a  less  uniform  appearance  is  presented. 

Emphysema  is  frequently  found  at  the  margins  of  the  lung  or  in 
the  neighborhood  of  the  infiltrated  areas.  Subpleural  and  interstitial 
emphysema  is  only  rarely  seen.  In  acute  cases,  the  bronchial  mucous 
membrane  is  reddened,  injected  and  swollen.     The  bronchi  contain 

1  Lord.  Infections  of  the  Respiratory  Tract  with  Influenza  Bacilli  and  Other  Organ- 
isms. Their  Clinical  and  Pathological  Similarity  and  Confusion  with  Tuberculosis, 
Boston  Med.  and  Surg.  Jour.,  May  11  and  18,  1905. 


BRONCHOPNEUMONIA  251 

a*  mucopurulent  or  purulent  secretion,  and  the  evidences  of  bronchial 
inflammation  can  be  followed  to  the  finest  ramifications  of  the  air 
passages.  In  long-standing  and  severe  cases,  the  bronchi  and  bron- 
chioles may  be  dilated.  The  pleura  is  much  less  frequently  involved  with 
bronchopneumonia  than  with  lobar  pneumonia.  Over  atelectatic  areas 
the  pleura  may  be  normal  or  slightly  clouded.  Overlying  broncho- 
pneumonic  areas  there  may  be  fibrinous,  serofibrinous  or  purulent 
pleurisy.     The  bronchial  glands  are  usually  enlarged,  soft  and  red. 

Microscopic  Examination. — In  the  centre  of  the  involved  area  is  a 
bronchus  or  bronchiole  with  its  lumen  plugged  with  pus  cells.  Its 
wall  is  swollen  and  partially  or  wholly  stripped  of  epithelium,  and 
may  be  irregularly  dilated.  In  the  absence  of  epithelium,  the  bron- 
chiole may  be  recognizable  as  such  only  from  the  presence  of  isolated 
circularly  disposed  muscle  fibers  and  elastic  tissue.  The  wall  of  the 
bronchiole  is  infiltrated  with  leukocytes.  The  walls  of  the  neighboring 
alveoli  are  swollen,  the  capillaries  are  distended  with  blood,  and  the 
alveolar  lumen  contains  leukocytes  and  desquamated  and  swollen 
epithelium.  Red  blood  corpuscles  are  absent  or  present  only  in  small 
numbers.  Fibrin  is  present,  but  much  less  abundantly  than  in 
croupous  pneumonia.  The  inflammatory  process  is  most  intense  in 
the  immediate  neighborhood  of  the  bronchial  ramifications,  wdiile 
toward  the  periphery  of  the  infiltrated  area  the  exudate  is  less  cellular. 
In  older  processes  the  cellular  elements  may  show  fatty  degeneration. 
Softening  of  isolated  alveolar  spaces  may  lead  to  the  production  of 
small  miliary  abscesses,  and  infiltration  of  the  involved  parts  with 
connective-tissue  cells  may  give  rise  to  focal  or  diffuse  induration. 

Pathologic  Similarity  of  the  Different  Infections. — Most  cases  of 
bronchopneumonia  are  due  to  mixed  infection  with  two  or  more 
organisms,  as  is  shown  by  the  results  of  cultures  taken  at  the  autopsy 
and  the  staining  of  sections  for  bacteria.  Neither  in  the  cases  of  mixed 
infection  with  different  organisms,  nor  in  those  in  which  one  group 
of  bacteria  predominates,  is  it  possible  to  note  any  striking  or  constant 
difference  in  the  character,  extent  or  intensity  of  the  bronchopneumonic 
process. 

Results  of  Bronchopneumonia. — In  many  cases,  the  exudate  is 
absorbed  or  expectorated,  and  the  condition  ends  in  symptomatic 
recovery.  The  conclusion  is  not  always  so  favorable,  and  the  patho- 
logic study  of  fatal  cases  offers  an  explanation  of  the  occasional 
persistence  of  symptoms  and  physical  signs  after  the  acute  infection 
has  subsided.  Gangrene  may  develop  but  is  uncommon.  Abscess 
formation  is  not  infrequent  in  fatal  cases.  Both  abscess  and  gangrene 
occur  more  frequently  in  the  aspiration  and  deglutition  forms  of 
bronchopneumonia. 

Among  85  cases  of  bronchopneumonia  coming  to  autopsy,  abscesses 
of  varying  extent  were  present  in  16  (macroscopic  in  10,  microscopic 
in  6).  Doubtless  in  many  instances  small  losses  of  pulmonary  sub- 
stance are  capable  of  complete  cicatrization.    There  is  a  compensatory 


252  DISEASES  OF  THE  LUNGS 

expansion  of  adjacent  parts  and  restoration  of  the  lung  to  complete 
functional  integrity.  In  other  cases,  small  pulmonary  defects  may 
never  be  fully  repaired  and  remain  as  permanent  pockets  for  the 
development  of  bacteria.  An  increase  in  the  interstitial  tissue  is  a 
frequent  finding  in  the  more  subacute  or  chronic  cases  of  broncho- 
pneumonia. The  formation  of  fibrous  tissue  takes  place  from  the 
interalveolar  septa,  the  interlobular,  peribronchial,  and  perivascular 
tissue.  In  this  series,  pulmonary  induration  was  found  in  31  cases 
(macroscopic  in  12,  microscopic  in  19).  In  8  of  the  85  cases  there 
were  well-marked  localized  abscesses,  pulmonary  induration  or  both. 

The  superior  lobes  or  the  apices  are  not  infrequently  the  site  of 
abscess  formation,  fibrous  induration  or  both,  in  consequence  of 
prolonged  or  recurrent  bronchopneumonia,  and  the  clinical  aspect 
may  then  closely  resemble  tuberculosis.  Thus,  in  4  of  the  8  cases, 
the  superior  lobes  were  involved.  In  one  case  there  was  an  area  of 
fibroid  tissue  at  both  apices,  the  left  apex  containing  an  irregular 
cavity  about  1  cm.  in  greatest  diameter,  with  trabeculated  walls  lined 
with  mucous  membrane,  which  was  apparently  continuous  with  a 
small  bronchus.  In  a  second  case,  the  greater  part  of  the  anterior 
portion  of  the  superior  lobe  of  the  left  lung  was  transformed  into  an 
irregular  cavity  containing  dirty,  reddish-brown,  foul  material,  lined 
with  a  firm  membrane  and  surrounded  by  indurated  tissue.  In  a 
third  case,  the  superior  lobe  over  a  large  part  of  its  extent,  especially 
the  superior  and  posterior  part,  was  resistant,  diminished  in  size 
and  extensively  transformed  into  a  blackish,  grayish,  fibrous-like 
tissue  of  a  very  tough  consistency,  and  showing  on  section  an  increase 
of  connective  tissue  and  obliteration  of  the  alveoli.  In  the  last  case, 
the  right  superior  lobe  wras  of  almost  board-like  hardness,  and  on 
section,  finely  granular,  pale  and  grayish.  On  microscopic  examina- 
tion, a  small  abscess  cavity  was  found  in  one  of  four  preparations  and 
increase  of  connective  tissue.  In  all  of  these  cases,  on  gross  inspection 
of  the  involved  regions,  the  inspection  of  thin  sections  made  with  the 
knife  and  microscopic  examination  of  material  from  the  abscess  wall 
or  the  areas  of  most  advanced  interstitial  changes,  there  was  no 
evidence  of  tuberculosis. 

Cylindrical  bronchiectasis  may  develop  early  in  the  course  of 
bronchopneumonia  as  a  result  of  infection  of  the  bronchial  wall  and 
violent  expulsive  efforts  with  cough.  This  is  more  likely  to  occur  in 
whooping  cough.  Bronchiectasis  develops  more  frequently,  however, 
in  association  with  abscesses  and  chronic  interstitial  changes  in  the 
lung  after  long-standing  infection.  Dilatation  of  the  terminal  bron- 
chioles may  occur  in  connection  with  bronchitis,  bronchiolitis,  and 
bronchopneumonia.  In  some  cases  the  condition  may  be  fitly 
described  as  "honey-comb"  lung. 

A  tuberculous  bronchopneumonia  may  develop  in  the  course  of 
simpler  infections  of  the  respiratory  tract,  and  is  not  very  infrequent 
following  measles  or  whooping  cough.     It  is,  of  course,  possible  that 


BRONCHOPNEUMONIA  253 

a  tuberculous  process  may  be  engrafted  on  a  simpler  infection,  but 
it  is  more  probable  that  such  processes  are  tuberculous  from  their 
inception,  a  latent  and  inactive  pulmonary  or  glandular  tuberculosis 
becoming  active  under  the  stimulus  of  the  acute  infection. 

Symptoms. — The  primary  form  of  bronchopneumonia  is  common 
in  infants,  but  is  rarely  seen  in  adults.  The  onset  is  abrupt  and  may 
be  accompanied  by  a  chill,  a  convulsion,  by  vomiting  or  pain  in  the 
side.  Cerebral  symptoms  may  be  a  prominent  feature.  A  history 
of  antecedent  bronchitis  is  lacking.  The  temperature  remains  con- 
stantly high  and  usually  terminates  abruptly  by  crisis.  Examination 
of  the  lungs  may  be  negative  or  there  may  be  signs  of  catarrh  of  the 
finer  tubes,  or  of  consolidation.  The  disease  is  rarely  fatal.  Recovery 
is  prompt  and  there  is  no  tendency  to  relapse.  The  clinical  features 
are  those  of  lobar  pneumonia. 

In  the  secondary  form  of  bronchopneumonia,  the  onset  is  rarely 
abrupt  or  with  a  chill.  The  child  is  perhaps  convalescing  from  measles 
or  whooping  cough,  but  the  bronchial  catarrh  still  persists,  and  after 
a  day  or  two  of  indisposition  and  indefinite  symptoms,  has  fever, 
rapid  pulse,  and  very  rapid  respiration.  There  are  copious  sweats 
and  marked  prostration.  The  progress  of  the  affection  is  then  rapid, 
and  the  cough  becomes  more  and  more  frequent,  hard,  painful,  and 
exhausting.  The  child  is  sleepless,  restless,  and  fussy.  The  pulse 
may  rise  rapidly  and  be  scarcely  perceptible  at  the  wrist,  and  the 
respirations  become  80  or  more  to  the  minute.  The  child's  face  and 
hands  are  very  hot  and  the  tongue  is  dry.  The  thirst  is  extreme. 
Vomiting  is  not  infrequent  and  there  may  be  constipation  or  diarrhea. 
Dyspnea  soon  becomes  a  most  prominent  and  distressing  feature. 
The  child  may  rapidly  become  apathetic  and  rouses  himself  and 
cries  only  during  a  paroxysm  of  cough  or  in  a  momentary  effort  to 
breathe.  As  the  urgency  of  the  initial  symptoms  abates,  and  the 
apathy  deepens,  paroxysms  of  cough  and  spasmodic  efforts  to  breathe 
are  less  frequent.  Signs  of  deficient  aeration  become  manifest  and 
progressively  increase.  The  face,  lips,  and  fingers  become  more  and 
more  cyanotic.  The  pulse  becomes  more  and  more  feeble,  the  respira- 
tion more  shallow.  Pallor  may  give  place  to  cyanosis.  The  extremities 
become  cool,  tracheal  rales  are  heard,  and  death  from  asphyxia  may 
occur  within  twenty-four  hours  of  the  onset.  Death  may  occur  in 
coma  or  with  convulsions  or  come  more  slowly.  In  infants  dying 
within  twenty-four  hours  of  the  onset,  atelectasis  alone  may  be  found 
in  the  lungs.  Older  children  succumb  less  rapidly  and  a  fatal  termina- 
tion may  be  delayed  for  some  days  to  several  weeks.  In  more  favor- 
able cases,  recovery  may  slowly  take  place,  but  convalescence  is  likely 
to  be  interrupted  by  relapses  and  the  patient  may  be  much  reduced 
in  weight  and  strength. 

In  adults  and  in  the  milder  types  of  infection  in  children,  the  lungs 
are  usually  invaded  by  extension  from  the  bronchi.  The  initial  symp- 
toms are  those  of  an  acute  bronchitis  on  which  the  pulmonary  process 


254  DISEASES  OF   THE  LUNGS 

is  insidiously  engrafted  or  its  onset  is  indicated  by  an  accession  of 
existing  symptom?.  A  chill  is  uncommon,  and  the  pleural  pain  of 
lobar  pneumonia  is  often  absent.  The  pulse  and  respiration  may 
become  more  rapid  and  there  may  be  an  increase  in  the  intensity  of 
the  cough,  dyspnea  or  cyanosis.  Herpes  is  rarely  observed.  The 
sputum  presents  no  characteristic  features  and  may  become  more  or 
less  abundant  after  the  onset  of  the  pneumonic  process.  It  is  usually 
made  up  of  discrete,  greenish-yellow,  purulent  masses  surrounded  by 
mucus  and  is  at  times  streaked  with  blood,  but  the  rusty  sputum  of 
lobar  pneumonia  is  not  observed. 

The  temperature  curve  is  not  characteristic.  Fever  is  usually 
present  and  may  be  higher  than  its  previous  level.  In  any  case  with 
the  clinical  features  of  bronchitis  in  which  the  fever  persists  beyond 
a  few  days,  the  presence  of  bronchopneumonia  should  be  suspected 
even  though  there  are  no  signs  of  solidification.  The  temperature 
may  be  only  slightly  elevated,  is  often  irregular  with  morning  remis- 
sions and  evening  exacerbations.  A  range  of  from  102°  to  104°  is 
not  uncommon.  It  may  be  normal  in  the  morning  and  elevated  at 
night.  In  severe  cases  it  may  remain  elevated  for  weeks,  and  its 
persistence  may  always  be  taken  to  indicate  that  the  infection  is  still 
an  active  one.  Defervescence  is  usually  by  lysis.  Sweating  is  fre- 
quently noted  during  the  disease.  The  temperature  may  remain 
normal  for  a  few  days,  to  be  followed  by  a  recurrence  of  fever  for  a 
variable  period. 

The  blood  usually  shows  a  leukocytosis. 

Physical  Signs. — There  may  be  no  positive  indications  whatever 
of  involvement  of  the  lung.  This  is  more  especially  the  case  in  rapidly 
fatal  infections  in  children  and  in  the  later  terminal  bronchopneumonias 
in  debilitated  subjects  in  whom  death  may  take  place  before  any 
definite  physical  signs  appear.  A  severe  diffuse  bronchitis  may  so 
mask  the  signs  of  bronchopneumonia,  as  to  make  it  impossible  to 
detect,  or  the  process  may  be  so  small  as  not  to  be  discoverable 
even  under  the  most  favorable  circumstances. 

On  inspection,  in  severe  cases  with  extensive  involvement,  respira- 
tory motion  is  frequent,  short,  and  superficial,  and  may  be  noted  to 
be  restricted  locally  over  those  parts  most  affected.  Thus  when  one 
or  both  lower  lobes  are  the  site  of  the  process,  the  upper  portions  of 
the  lungs  on  the  same  or  on  both  sides  may  be  more  mobile.  With 
wide-spread  collapse  or  with  capillary  bronchitis  and  bronchopneu- 
monia, especially  in  infants  with  elastic  thoracic  walls,  there  may  be 
marked  inspiratory  retraction  of  the  lower  sternal  region  and  the 
costal  margin  in  consequence  of  the  deficient  expansion  of  the  lower 
lobes.  The  cervical  veins  may  be  swollen  from  congestion  in  the 
pulmonary  circuit.  Pulmonary  collapse  in  the  neighborhood  of  the 
heart  may  increase  the  area  of  visible  cardiac  pulsation,  or  pulmonary 
inflation  may  diminish  it. 

The  recognition  of  an  initial  collapse  of  the  lung  is  difficult  or 


BRONCHOPNEUMONIA  255 

impossible.  A  change  in  the  contour  of  the  lower  boundary  of  the 
lung  outlined  by  percussion,  relative  dulness  with  a  slightly  tympanitic 
quality  and  diminished  respiration  without  rales  are  suggestive  evi- 
dence. A  disappearance  of  these  signs  with  the  appearance  of  fine 
crepitations  after  a  deep  inspiration  is  the  only  positive  indication. 

On  auscultation,  rales  are  the  most  constant  finding  in  cases  with 
bronchopneumonia,  and  vary  in  their  character  and  distribution 
with  the  nature  and  extent  of  the  process.  An  accompanying  bronchitis 
of  the  larger  or  smaller  tubes  may  be  indicated  by  sonorous  or  sibilant 
dry  rales,  or  by  fine,  medium  or  coarse  non-consonating  moist  rales. 
Involvement  of  the  lung  may  modify  the  character  of  the  moist  rales 
and  make  them  more  clear  cut,  sharp,  and  distinct,  of  the  so-called 
consonating  quality,  from  which  alone  and  without  other  signs,  the 
existence  of  pulmonary  invasion  may  be  suspected.  This  distinction 
between  the  non-consonating  rales  of  bronchitis  and  the  consonating 
rales  of  pulmonary  consolidation  is  sufficiently  obvious  in  certain 
cases  to  make  it  of  value  in  diagnosis,  but  it  is  often  difficult  or  impos- 
sible of  appreciation.  The  persistence  of  rales  at  one  place  in  the  lung 
may  also  be  taken  as  probable  evidence  of  pulmonary  changes  in  the 
involved  region. 

Bronchial  breathing  may  be  present  without  dulness  if  the  consoli- 
dation is  centrally  placed.  It  may  be  necessary  to  ask  the  patient  to 
cough,  and  thus  free  the  bronchi  of  secretion  in  order  to  bring  it  out. 
The  whisper  may  be  increased  and  have  a  bronchial  quality.  Increase 
of  voice  and  tactile  fremitus  may  also  be  noted. 

Dulness  may  or  may  not  be  present.  Owing  to  the  resonance  of 
the  chest  in  children,  slight  changes  in  the  note  may  be  difficult  of 
appreciation.  Light  percussion  with  a  short,  sharp,  quick  stroke  is 
more  likely  to  lead  to  the  detection  of  changes  from  superficial  areas, 
while  heavy  percussion  may  be  needed  for  central  areas.  The  percus- 
sion note  over  different  parts  of  the  chest  in  the  neighborhood  of  a 
suspected  area  should  be  carefully  compared  as  well  as  over  sym- 
metrical parts  of  the  two  sides  in  order  to  avoid  error  in  case  the 
consolidation  is  bilateral. 

Considerable  variation  in  the  physical  signs  is  observed  from  day 
to  day.  Plugging  of  the  bronchi  with  tenacious  secretion  may  lead 
to  the  apparent  disappearance  of  a  small  focus,  which  later  reappears. 
The  invasion  of  new  and  nearby  or  remote  territory  is  not  infrequent. 
The  extent  of  the  process  varies  from  areas  no  larger  than  the  bell 
of  the  stethoscope  to  the  involvement  of  the  greater  part  or  the 
whole  of  one  or  more  lobes.  With  numerous  and  closely  aggregated 
or  confluent  areas  the  dulness,  bronchial  breathing,  increase  of 
voice,  whisper  and  tactile  fremitus  may  be  as  marked  as  with  lobar 
pneumonia. 

Complications  and  Sequelae. — Bronchopneumonia  is  invariably 
accompanied  by  bronchitis,  and  laryngitis  is  not  uncommon,  especially 
when  the  disease  complicates  diphtheria  or  measles.    There  may  then 


256  DISEASES  OF  THE  LUNGS 

be  hoarseness,  aphonia,  and  severe  dyspnea  of  the  inspiratory  type. 
A  fatal  laryngeal  stenosis  may  be  the  result.  Croupous  pneumonia 
may  coexist,  and  even  at  autopsy  it  may  be  difficult  to  differentiate 
between  confluent  bronchopneumonia  and  lobar  pneumonia.  A  slum- 
bering tuberculous  process  may  be  awakened  into  activity.  Pleuritis 
is  less  common  than  with  lobar  pneumonia,  but  fibrinous,  serofibrinous 
or  purulent  forms  occur  and  may  be  difficult  of  recognition.  Pneumo- 
thorax is  rare,  as  are  also  pericarditis  and  endocarditis. 

It  is  not  very  uncommon  for  an  acute  bronchopneumonia  to  initiate 
a  persistent  pulmonary  infection,  as  already  mentioned  under 
Pathology.  A  persistent  cough,  with  or  without  purulent  sputum, 
may  be  the  only  symptom,  and  physical  examination  may  fail  to 
detect  the  site  of  the  pulmonary  process.  Emphysema  is  likely  to 
complicate  the  chronic  infections. 

The  subsequent  course  of  a  persistent  pulmonary  infection  is  very 
variable.  It  may  slowly  subside  and  end  in  full  recovery,  or  slowly 
progress,  interrupted  at  longer  or  shorter  intervals  by  acute  symptoms 
as  the  disease  lights  up  in  previously  uninvolved  parts  of  the  lung. 
In  some  cases,  relapses  occur  irregularly  at  intervals  of  days,  weeks, 
months  or  years,  and  the  patient  then  usually  presents  the  evidences 
of  a  persistent  infection  during  the  intervals  of  freedom  from  the 
acute  exacerbations.  The  clinical  features  are  those  of  chronic  inter- 
stitial pneumonia  with  bronchiectasis  or  abscess  formation,  and  the 
influenza  bacillus  may  be  found  in  the  sputum.  It  is  uncertain, 
however,  whether  this  organism  is  to  be  regarded  as  more  than  a  con- 
tributing factor  in  the  presence  of  mixed  infection.  The  lower  lobes 
are  usually  the  site  of  the  infection  and  should  be  examined  with 
special  care.  Examination  by  means  of  the  .r-rays  may  lead  to  the 
detection  of  a  process  not  otherwise  to  be  found. 

As  compared  with  lobar  pneumonia,  the  physical  signs  of  broncho- 
pneumonia subside  much  more  gradually.  Even  after  a  long  period 
of  slow  resolution,  complete  symptomatic  recovery  may  yet  occur. 
In  one  case  of  influenza  bronchopneumonia,  the  bronchial  breathing 
disappeared  only  after  six  months,  and  yet  finally  the  cough,  expectora- 
tion and  physical  signs  completely  disappeared. 

Types  of  Bronchopneumonia. — In  Children. — The  primary  form  of 
bronchopneumonia  is  seen  as  a  rule  only  in  children.  Whether  primary 
or  secondary,  the  disease  is  characterized  by  its  severe  course,  and  the 
younger  the  child,  the  more  serious  is  it  likely  to  be.  This  is  to  be 
ascribed  to  the  greater  readiness  with  which  the  finer  bronchi  become 
occluded  in  youth,  and  the  lack  of  muscular  strength  to  expel  the 
exudate.    Sputum  is  usually  absent  in  children  under  three  years  of  age. 

In  the  Aged. — The  bronchopneumonia  is  almost  invariably  secondary, 
and  the  pulmonary  features  are  likely  to  be  insignificant.  Cough, 
expectoration,  dyspnea,  and  fever  may  be  absent.  The  condition  is 
likely  to  be  terminal  and  of  short  duration.  It  is  frequently  over- 
looked during  life  and  first  discovered  at  autopsy. 


BRONCHOPNEUMONIA  257 

Following  the  Infectious  Fevers. — The  younger  the  child,  the  greater 
the  danger  of  the  development  of  bronchopneumonia  as  a  complica- 
tion of  measles.  In  Bartels'  series  of  573  cases  of  measles,  68  (12  per 
cent.)  had  pulmonary  complications.  Of  those  under  one  year,  nearly 
20  per  cent,  were  affected,  while  only  13  per  cent,  of  those  from  one 
to  five  years,  and  only  about  10  per  cent,  of  those  from  five  to  ten 
years.  Death  was  due  to  this  cause  in  nearly  80  per  cent,  of  all  fatal 
cases.  The  mortality  is  higher  the  younger  the  child,  and  may  reach 
100  per  cent,  in  patients  under  one  year.  Bronchopneumonia  develops 
at  any  stage  of  the  disease,  but  most  often  during  or  after  the  dis- 
appearance of  the  efflorescence.  In  rare  instances,  an  interval  of  some 
weeks  may  elapse.  The  patients  may  be  apparently  well  with  the 
exception  of  a  persistent  bronchial  catarrh.  The  clinical  aspect 
does  not  differ  from  that  in  other  types  of  the  disease.  Convalescence 
is  at  times  much  prolonged.  A  smouldering  tuberculous  process  may 
be  ligfited  into  activity  by  the  infection. 

Bronchopneumonia  complicating  whooping  cough  develops  most 
often  in  young  subjects,  and  most  commonly  during  the  spasmodic 
stage  of  the  disease.  It  is  likely  to  run  a  long  course,  and  may  end  in 
recovery  or  a  chronic  and  persistent  infection  with  permanent  changes 
in  the  lung. 

Bronchopneumonia  complicating  diphtheria  usually  arises  by  aspira- 
tion of  infected  material  from  the  upper  parts  of  the  respiratory  tract, 
but  is  at  times  due  to  direct  extension  of  the  disease  from  the  bronchi. 
The  diphtheria  bacillus  alone  may  be  concerned,  but  mixed  infections 
are  common,  and  other  organisms  than  the  diphtheria  bacillus  may  be 
wholly  responsible.1  Fibrinous  casts  of  the  bronchi  are  at  times 
expectorated.  Necrosis  leading  to  abscess  formation  is  not  infrequent. 
Recovery  may  occur,  but  convalescence  is  usually  slow,  and  chronic 
interstitial  pneumonia,  abscess,  gangrene  or  bronchiectasis  may 
follow  the  infection. 

Plague  Pneumonia  (The  Black  Death). — The  black  death  of  the 
middle  ages  is  to  be  regarded  as  plague  pneumonia.  True  plague 
pneumonia  may  be  primary  or  secondary.  It  is  fortunately  uncommon, 
comprising  usually  only  about  5  per  cent,  of  the  cases,  but  is  highly 
contagious.  Plague  bacilli  may  be  disseminated  into  the  surrounding- 
air  during  attacks  of  cough,  as  shown  by  Strong,2  and  the  wearing  of 
masks  by  those  exposed  and  the  sterilization  of  infected  clothing  are 
important  preventive  measures.  Whether  primary  or  secondary, 
the  occurrence  of  pneumonic  plague  may  have  an  important  bearing 
on  the  character  of  an  epidemic  and  increase  the  incidence  of  the 
pulmonary  form  among  those  attacked. 

The  pulmonary  infection  is  lobular,  and  disseminated  areas  vary  in 

1  Wright  and  Stokes  (Boston  Med.  and  Surg.  Jour.,  April  4,  1S95)  found  the  diphtheria 
bacillus  in  18  of  19  cases,  in  8  in  pure  culture;  Pearce  (ibid.,  December  2,  1897)  in  63 
of  73  cases,  and  in  pure  culture  in  17. 

2  Jour.  Amer.  Med.  Assoc,  October  14,  1911. 

17 


258  DISEASES  OF   THE  LUNGS 

size  from  that  of  a  pea  to  an  egg,  while  confluent  foci  may  embrace 
the  greater  part  of  a  lobe.  The  involved  regions  are  likely  to  be  in- 
tensely hemorrhagic  and  contain  pest  bacilli  in  large  numbers. 
Hemorrhages  may  be  found  in  other  parts  of  the  body,  especially  in 
the  pleura.  Bronchitis  of  varying  degrees  of  intensity  accompanies 
the  process.  The  bronchial  glands  are  enlarged,  soft,  edematous  and 
byperemic,  and  are  to  be  regarded  as  secondary  buboes.  The  spleen 
is  enlarged.    Death  is  due  to  toxemia. 

Primary  pest  pneumonia  is  an  infection  of  the  lung  as  the  primary 
seat  of  the  disease,  and  is  unpreceded  by  primary  buboes  or  a  primary 
carbuncle.  Only  a  few  cases  have  been  accurately  recorded.  It  arises 
by  inhalation  of  the  organisms  and  has  been  produced  experimentally 
by  Wyssokowitsch  and  Zabolotny1  by  insufflation  of  pest  bacilli  into 
the  trachea  of  a  monkey,  and  by  Goss2  by  forcing  guinea-pigs  to  inhale 
a  fine  spray  containing  the  organisms.  In  the  unfortunate  case  of 
Dr.  Screiber,  reported  by  Berestnew,3  pulmonary  infection  was  thought 
to  have  taken  place  by  the  aspiration  of  organisms  through  a  pipette. 
The  incubation  period  is  probably  one  week  or  less,  and  the  disease 
usually  begins  suddenly  with  a  chill  or  chilliness  followed  by  fever. 
Malaise,  headache,  and  vomiting  are  of  varying  degrees  of  intensity. 
The  fever  is  continuous  or  remittent.  Distressing  and  frequent 
cough,  constant  and  increasing  dyspnea  and  cyanosis  are  important 
symptoms.  Pleural  pain  is  often  present.  The  sensorium  is  usually 
undisturbed,  but  in  some  cases  there  is  delirium.  Conjunctivitis 
may  be  present  as  in  the  bubonic  form.  Herpes  is  absent.  The 
sputum  may  be  absent,  scanty  or  abundant,  mucoid  or  mucopurulent, 
blood-streaked  or  frankly  hemorrhagic.  Frothy,  liquid,  bloody  sputum 
is  the  most  striking  single  feature  of  the  disease  and  lacks  the  tenacious 
quality  of  ordinary  pneumonic  sputum.  On  examination,  there  may 
be  only  the  signs  of  bronchitis,  but  in  some  cases  more  obvious  evi- 
dences of  infiltration  as  in  other  forms  of  bronchopneumonia.  The 
spleen  is  usually  palpable  to  two  or  more  fingers'  breadth  below  the 
costal  margin.  Pest  bacilli  may  be  found  in  the  expectoration  in 
enormous  numbers  and  also  in  the  circulating  blood.  There  are  no 
authentic  cases  of  recovery  from  plague  pneumonia,  and  death  usually 
occurs  from  the  fourth  to  the  sixth,  but  may  come  as  early  as  the  second 
or  as  late  as  the  fourteenth  or  fifteenth  day  of  the  disease.  The 
diagnosis  may  be  made  by  establishing  a  source  of  contagion,  by  the 
bloody  sputum,  presence  of  plague  bacilli  in  the  blood  and  expecto- 
ration, and  the  rapid  and  fatal  course.  The  complement-fixation  test 
is  positive  in  pest,  but  may  not  appear  until  late  in  the  disease.4 

Secondary  pneumonia  in  plague  may  be  lobar  and  due  to  the  pneumo- 

1  Recherches  sur  la  peste  bubonique,  Ann.  de  l'lnst.  Past.,  1897. 

2  Arch.  d.  sc.  biologiques,  St.  Petersburg,  1908,  vol.  xiii. 

*  Sur  les  cas  de  peste  survenus  au  laboratoire  du  fort  Alexandre  ler.  a  Oronstadt  en 
fevrier,  1907,  Arch.  d.  sc.  biologiques,  St.  Petersburg,  1908,  vol.  xiii. 

•  Amake,  Cetitralbl.  f.  Bakt.,  1  Orig.,  Bd.  li,  H.  6. 


BRONCHOPNEUMONIA  2;")!) 

coccus,  but  bronchopneumonia  is  the  usual  type  and  may  be  caused 
by  pest  bacilli  or  other  organisms.  True  secondary  plague  pneumonia 
may  result  from  the  lodgment  in  the  lung  of  infected  emboli  or  the 
aspiration  of  material  containing  pest  bacilli  dislodged  from  an 
ulcerated  tonsillar  bubo.  As  with  bronchopneumonia  complicating 
other  grave  infections,  secondary  plague  pneumonia  is  usually  unde- 
tected during  life,  and  is  first  discovered  at  the  postmortem  examina- 
tion. In  some  cases  it  may  be  suspected  from  the  cough,  dyspnea, 
and  cyanosis  or  established  on  physical  examination.  The  sputum 
usually  lacks  characteristic  features  and  is  like  that  in  ordinary 
bronchopneumonia.  It  may  be  bloody,  but  the  frankly  hemorrhagic 
expectoration  of  the  primary  form  is  rarely  seen.  The  embolic  form 
may  occur  early  in  the  disease  and  involves  any  part  of  the  lung,  while 
aspiration  plague  pneumonia  is  a  late  manifestation  and  predomi- 
nately affects  the  lower  lobes.  The  outlook  is  grave,  but  recovery 
occasionally  occurs. 

Diagnosis. — The  insidious  onset,  irregular  course  and  frequent 
absence  of  definite  physical  signs  make  the  diagnosis  of  broncho- 
pneumonia difficult  and  at  times  impossible.  Bronchopneumonia 
practically  always  complicates  capillary  bronchitis  and  may  therefore 
be  assumed  to  be  present  in  this  disease  in  the  absence  of  more  definite 
signs.  A  bronchopneumonia  may  be  suspected  also  in  the  presence  of 
a  simple  bronchitis,  when  the  fever  persists  longer  than  a  few  days, 
when  in  the  acute  attack  rales  are  localized  over  one  lobe  or  one  lung, 
or  persist  in  one  place  longer  than  elsewhere,  or  when  without  change 
in  the  local  signs  there  is  a  sudden  increase  in  toxic  symptoms  and 
elevation  of  the  temperature,  pulse,  and  respiration.  Urgent  dyspnea 
and  cyanosis  are  rarely  present  in  simple  bronchitis. 

The  distinction  between  bronchopneumonia  and  lobar  pneumonia 
is  usually  not  difficult.  It  is  to  be  remembered  that  primary  broncho- 
pneumonia is  very  uncommon  in  adults,  and  occurs  chiefly  in  children 
under  three  years.  At  this  age,  the  symptoms  of  primary  broncho- 
pneumonia and  lobar  pneumonia  are  the  same,  but  the  former  is  much 
more  frequent,  and  physical  signs,  if  present,  may  indicate  bilateral 
and  multiple  areas  of  consolidation.  A  primary  confluent  broncho- 
pneumonia can  hardly  be  distinguished  from  lobar  pneumonia. 
Whether  in  adults  or  in  children,  secondary  bronchopneumonia  occur- 
ring in  the  course  of  or  during  convalescence  from  another  affection, 
of  insidious  onset,  without  chill,  absence  of  herpes,  slow  course,  lack  of 
rusty  sputum,  presence  of  bilateral  and  multiple  areas  of  consolida- 
tion, defervescence  by  lysis,  slow  resolution  and  tendency  to  relapse 
is  usually  readily  differentiated  from  lobar  pneumonia. 

Bronchopneumonia  may  be  confused  with  an  encysted  pleural 
exudate  when  the  bronchi  leading  to  the  consolidated  area  are  plugged. 
There  may  then  be  dulness,  diminished  or  absent  breathing,  voice, 
whisper  and  tactile  fremitus,  but  the  heart  is  not  displaced,  Grocco's 
paravertebral  triangle  of  dulness  is  absent,  the  percussion  note  is 


260  DISEASES  OF  THE  LUNGS 

dull  rather  than  flat,  and  the  presence  of  air-holding  tissue  may  be 
established  all  about  the  involved  region,  an  uncommon  event  with 
pleural  exudates,  which  usually  reach  to  the  inferior  margin  of  the 
pleural  cavity.  A  change  in  the  signs  after  the  bronchi  are  freed  of  the 
obstruction  by  cough  may  make  the  situation  clear.  An  exploratory 
puncture  should  not  be  delayed  in  doubtful  cases. 

A  simple  bronchopneumonia  may  be  closely  simulated  by  the  pul- 
monary form  of  miliary  tuberculosis,  which  also  at  times  follows 
measles  and  whooping  cough,  and  is  accompanied  by  cough,  mucopuru- 
lent and  at  times  blood-streaked  sputum  (usually  without  tubercle 
bacilli),  dyspnea,  cyanosis,  and  signs  of  bronchitis.  Evidence  of  tuber- 
culosis in  the  family  or  the  past  history,  fever  preceding  the  onset  of 
the  pulmonary  symptoms,  the  presence  of  a  local  tuberculous  lesion 
in  the  apex  of  the  lung,  in  the  glands,  the  choroid  or  elsewhere,  dyspnea 
and  cyanosis  out  of  proportion  to  the  local  signs,  or  cerebral  symptoms 
may  suggest  the  tuberculous  nature  of  the  affection.  As  the  two 
diseases  may  be  associated,  the  diagnosis  is  not  infrequently  difficult 
or  impossible  without  definite  evidence  of  tuberculosis. 

It  is  especially  in  the  more  persistent  or  relapsing  types  of  the  sim- 
pler infections  that  the  question  of  tuberculosis  arises.  Broncho- 
pneumonia due  to  other  organisms  than  the  tubercle  bacillus  shows 
a  tendency  in  a  small  proportion  of  the  cases  to  end  in  permanent 
damage  to  the  pulmonary  substance,  and  the  patient  then  presents 
himself  with  a  history  of  cough  and  expectoration  for  a  few  weeks,  or 
it  may  be  for  months.  There  may  be  suggestive  points  in  the  history. 
Tuberculosis  in  the  family  or  known  opportunity  for  contagion,  a 
history  of  primary  pleurisy  or  of  hemoptysis  out  of  a  clear  sky  may 
suggest  tuberculosis.  If  the  cough  began  without  preceding  catarrhal 
symptoms,  it  is  also  suggestive,  but,  on  the  contrary,  little  evidence 
against  tuberculosis  can  be  ascribed  to  the  history  of  a  "cold"  wdiich 
leaves  the  patient  with  a  persistent  cough.  Many  cases  of  tuberculosis 
begin  in  this  way,  a  previously  inactive  or  slowly  advancing  lesion 
being  thus  excited  to  more  rapid  progress.  Concerning  the  course  of 
the  disease,  it  may  be  said  that  the  chronic  non-tuberculous  infections 
seldom  tend  toward  a  fatal  termination,  but  rather  remain  stationary 
or  slowly  progress  with  exacerbations  and  remissions,  but  without 
serious  impairment  of  the  general  nutrition.  The  progress  of  the  tuber- 
culous cases  is  more  rapidly  downward,  and  loss  of  weight  and  strength, 
night  sweats,  and  evening  rise  of  temperature  are  more  common.  On 
general  examination,  the  finding  of  phlyctenular  conjunctivitis,  cor- 
neal scars  (if  trauma,  gonorrhea  or  syphilis  can  be  excluded),  enlarged 
cervical  glands  or  scars  of  previous  trouble,  ischiorectal  abscess  or 
fistula  are  significant.  On  the  part  of  the  lungs,  the  non-tuberculous 
infections  more  frequently  involve  the  inferior  lobes,  while  the  tuber- 
culous invasion  is  commonly  apical.  Clinical  and  postmortem  experi- 
ence indicates  that  apical  lesions  are  so  rarely  due  to  other  causes 
than  the  tubercle  bacillus,  that  they  should  be  regarded  as  tuberculous 


BRONCHOPNEUMONIA  261 

until  they  can  be  proved  otherwise,  and  no  clinical  diagnosis  of  non- 
tuberculous  apical  disease  can  safely  be  made  until  this  diagnosis  is 
confirmed  by  negative  tests  with  tuberculin. 

Prognosis. — This  is  very  difficult  to  estimate  because  of  the  large 
number  of  cases  in  which  the  condition  is  overlooked.  In  the  primary 
form  in  children  the  outlook  is  favorable.  The  mortality  in  secondary 
bronchopneumonia  is  highest  at  the  extremes  of  age.  In  children  it 
varies  in  different  series  from  30  to  75  per  cent,  of  the  cases,  and  is 
highest  in  those  who  are  poorly  nourished,  or  enfeebled  by  rickets, 
syphilis,  diarrhea,  or  prolonged  febrile  disease.  Fat  children  are 
said  to  stand  bronchopneumonia  badly.  In  adults  with  such  debili- 
tating conditions  as  malignant  disease,  broken  cardiac  compensation, 
chronic  nephritis,  cerebral  hemorrhage,  brain  tumor,  pernicious  and 
severe  secondary  anemia,  leukemia,  exophthalmic  goitre,  diabetes,  etc., 
bronchopneumonia  is  extremely  fatal.  The  outlook  is  more  unfavor- 
able with  an  extensive  process,  very  rapid  respiration,  marked  cyanosis, 
apathy,  and  cerebral  symptoms.  Aspiration  or  deglutition  pneumonia 
is  a  very  fatal  form.  Among  339  cases  of  bronchopneumonia  at  the 
Massachusetts  General  Hospital  where  children  comprise  only  a  small 
proportion  of  the  admissions,  there  were  89  deaths,  a  mortality  of 
26  per  cent.,  which  is  higher  than  that  for  lobar  pneumonia  during 
the  same  period.  The  duration  of  the  disease  is  longer  than  with  lobar 
pneumonia.  No  definite  statement  concerning  the  duration  can  be 
made,  but  the  acute  symptoms  seldom  subside  within  less  than  two 
weeks,  and  an  equal  period  may  elapse  before  resolution  is  complete  in 
favorable  cases.  For  the  persistent  and  relapsing  forms,  no  time  limit 
can  be  set. 

Prophylaxis. — As  undernourishment  is  a  predisposing  factor,  proper 
and  abundant  food  and  fresh  air  may  be  expected  to  diminish  the  inci- 
dence of  the  disease.  If  there  is  an  infection  of  the  respiratory  tract, 
special  care  should  be  exercised  to  avoid  exposure  to  cold  or  draught 
when  insufficiently  clad,  and  rapid  cooling  of  the  body  when  over- 
heated. Pure  air  free  from  dust,  and  an  equable  temperature  should 
be  secured  in  the  house.  The  child  should  not  be  taken  out  on  windy 
and  dusty  days,  and  as  a  precaution,  when  out,  it  is  well  for  the  child 
to  wear  a  veil.  Measures  directed  toward  limiting  the  spread  of  the  in- 
fectious fevers  will  do  much  to  diminish  the  number  of  cases  of  broncho- 
pneumonia. Careful  cleansing  of  the  mouth  and  teeth  during  the 
fevers  or  in  serious  illness  of  any  sort,  and  preceding  general  anesthesia 
and  the  postponement,  when  possible,  of  anesthesia  when  the  patient 
has  tonsillitis,  bronchitis  or  other  respiratory  infection,  will  diminish 
the  number  of  cases  of  aspiration  pneumonia.  The  stomach  should 
be  empty  before  the  patient  is  anesthetized.  In  stupor  or  unconscious- 
ness from  any  cause,  the  patient  should  be  carefully  fed,  the  head 
should  be  turned  so  that  saliva  and  mucus  may  escape  freely  from  the 
mouth,  and  when  vomiting  occurs  the  patient  should  be  turned  on  the 
side  so  that  the  vomitus  may  be  expelled.    Special  care  should  be  exer- 


262  DISEASES  OF  THE  LUNGS 

cised  to  avoid  the  aspiration  of  infected  material  during  operations 
on  the  nose,  mouth  or  larynx.  In  all  conditions  in  which  atelectasis 
is  known  to  be  present,  or  likely  to  develop,  the  position  of  the  patient 
should,  if  possible,  be  frequently  changed. 

Early  and  careful  attention  to  bronchitis,  especially  in  infants, 
will  do  much  to  prevent  the  development  of  bronchopneumonia.  All 
cases  of  respiratory  infection  should  be  regarded  as  presenting  the 
possible  danger  of  contagion,  and  isolation  should,  as  far  as  possible, 
be  secured. 

Treatment. — There  is  no  specific  treatment,  and  reliance  must  be 
placed  principally  on  rest,  fresh  air,  and  proper  feeding.  The  patient 
should  be  abed  and  absolutely  at  rest  while  there  is  fever.  Frequent 
changes  of  position,  as  already  mentioned,  may  favorably  influence 
atelectasis.  The  patient's  room  should  be  well  lighted  and  well  ven- 
tilated and  an  open  fire-place  improves  the  circulation  of  air.  An 
abundance  of  fresh  air  should  be  secured  by  night  as  well  as  by  day 
by  throwing  the  windows  open,  care  being  taken,  however,  not  to  have 
the  patient  directly  exposed  to  a  strong  current  of  air  and  that  the 
bed  clothes  are  not  thrown  off.  In  infants  at  the  breast,  the  dyspnea 
may  prevent  breast  feeding,  and  the  milk  may  then  be  pumped  from 
the  breast  and  fed  with  a  spoon.  To  infants  who  are  artificially  fed, 
properly  modified  milk  should  be  given.  There  are  no  special  indica- 
tions concerning  the  diet,  and  the  patient  should  be  given  as  much 
of  simple  and  nutritious  food  as  he  can  digest,  the  effort  being  made 
in  poorly  nourished  patients  to  improve  the  general  condition.  In 
the  early  stages  of  the  disease,  while  there  is  fever  and  toxemia,  the 
diet  may  well  be  limited  to  milk  and  milk  preparations,  broths  and 
albumin  water.  The  child  should  be  encouraged  to  drink  water 
freely. 

In  mild  cases  such  simple  measures  suffice.  Attention  should  be 
paid  to  the  bowels,  and  if  necessary,  rectal  enemata  or  mild  laxatives 
may  be  given.  If  there  is  pain,  distressing  dyspnea  and  incessant 
and  unproductive  cough,  opium  may  be  given  in  the  form  of  codeine 
gr.  2V  (0.0032  gm.),  heroin  gr.  T^  (0.00065  gm.),  or  paregoric  m. 
3  to  5  (0.2  to  0.3  c.c.)  to  an  infant  of  six  months,  but  should  not  be 
used  unless  there  is  some  special  indication,  and  then  only  cautiously. 
Local  applications  to  the  chest  are  now  little  used.  Flax-seed  meal 
or  ice  poultices,  oil  silk  or  cotton  batting  jackets,  or  Priessnitz's  appli- 
cations, by  constricting  the  chest  and  diminishing  the  respiratory 
motion,  may  do  more  harm  than  good.  Counterirritation  with  dry 
cups,  mustard  paste  or  other  means  irritates  the  skin,  and  may  add  to 
the  discomfort  of  the  patient.  If  the  pulse  shows  signs  of  weakening, 
digitalis,  camphor,  and  caffeine  may  be  used.  With  distressing  cough, 
mucus  rattling  in  the  bronchi,  increasing  dyspnea  and  restlessness,  aro- 
matic spirits  of  ammonia  may  be  used  as  an  expectorant  in  infants  and 
ammonium  chloride  in  older  children.  When  the  secretion  is  abundant 
and  the  cough  feeble,  syrup  of  ipecac  may  be  used  as  an  emetic  to  aid 


BRONCHOPNEUMONIA  263 

in  the  expulsion  of  the  mucus,  but  should  not  be  given  if  the  child 
is  greatly  prostrated.     Inhalations  of  oxygen  may  also  be  useful. 

Attacks  of  cardiac  weakness  with  cyanosis  and  mucus  rattling  in  the 
bronchi  may  be  combated  with  a  hot  mustard  bath  (four  tablespoon sful 
of  powdered  mustard  to  four  gallons  of  water),  digitalis,  camphor, 
caffeine,  and  inhalations  of  oxygen.  For  nervous  symptoms  with 
hyperpyrexia,  the  cold  bath  or  cold  pack  may  be  used.  When  the  cold 
bath  is  used,  the  temperature  of  the  water  should  be  gradually  low- 
ered for  children,  from  tepid  to  75°  or  80°,  the  peripheral  circulation 
being  maintained  during  the  bath  by  massage  of  the  extremities  and 
the  body  and  the  application  of  heat  to  the  extremities  after  the  bath. 
If  the  prostration  is  extreme,  it  is  best  not  to  use  cold  applications, 
and  the  hot  mustard  bath  may  be  substituted. 

In  protracted  and  relapsing  types  of  bronchopneumonia,  every 
effort  should  be  made  to  improve  the  general  health.  This  is  usually 
best  done  by  treating  the  patient  as  if  for  tuberculosis  by  rest,  fresh 
air,  and  extra  feeding. 


CHAPTER  XIV. 
SUBACUTE  AND  CHRONIC  INDURATIVE  PNEUMONIA. 

Conditions  termed  cirrhosis  of  the  lung,  pulmonary  sclerosis, 
fibroid  phthisis,  cirrhotic  or  fibroid  pneumonia  are  also  included  under 
this  heading.  By  it  is  understood  a  fibroid  change  starting  about 
the  bronchi  or  the  bloodvessels,  in  the  interlobular,  the  interalveolar 
or  the  subpleural  tissue.  Subacute  and  chronic  types  are  at  times 
described  separately,  but  as  the  causes  are  for  the  most  part  the  same, 
and  the  two  forms  represent  but  different  stages  in  the  same  patho- 
logic process,  their  separate  consideration  would  entail  needless  repeti- 
tion.   A  useful  division  may  be  made  into  diffuse  and  local  induration. 

Etiology. — The  causes  are  many  and  difficult  to  classify.  In  indi- 
vidual cases  it  is  often  difficult  to  determine  the  character  of  the 
initial  process,  and  in  many  instances  the  condition  seems  to  have 
had  an  insidious  onset.  The  essential  factor  is  probably  a  subacute  or 
chronic  infection,  the  exact  nature  of  which  it  may  be  impossible  to 
determine,  since  the  infecting  organisms  may  die  out,  leaving  only 
scar  tissue  as  an  indication  of  their  previous  presence.  Secondary 
invasion  with  other  organisms  may  take  place,  and  thus  mask  the 
original  nature  of  the  process. 

The  histologic  study  of  postmortem  specimens  shows  connective 
tissue  formation  most  frequently  in  process  of  formation  about  tuber- 
culous areas,  in  organizing  bronchopneumonia  and  lobar  pneumonia, 
and  in  parts  of  the  lung  adjacent  to  an  infected  pleura,  and  it  is 
therefore  reasonable  to  refer  an  already  established  induration  in 
many  instances  to  such  causes. 

Diffuse  induration  is  commonly  due  to  organized  croupous  or  bron- 
chopneumonia or  to  the  extension  of  an  infection  from  a  purulent  pleu- 
ritis.  In  clinical  cases,  the  development  of  induration  after  croupous 
pneumonia  is  observed  only  in  rare  instances.  Among  1000  cases  of 
genuine  croupous  pneumonia,  Frankel1  had  the  opportunity  to  observe 
at  autopsy  a  termination  in  induration  and  contraction  in  only  seven. 
Among  210  cases  at  the  Massachusetts  General  Hospital  showing 
genuine  croupous  pneumonia  at  autopsy,  or  referring  their  pul- 
monary symptoms  to  what  may  be  interpreted  as  lobar  pneumonia, 
there  were  10  instances  of  organizing  or  indurative  pneumonia. 
Bronchopneumonia  is  a  more  frequent  cause,  pulmonary  indura- 
tion being  noted  macroscopically  (as  mentioned  in  the  section  on 
Bronchopneumonia)  in  12  of  85  cases  coming  to  postmortem  exami- 

1  Spec.  Path.  u.  Ther.  d.  Lungenkrankheiten,  1904,  p.  452. 


SUBACUTE  AND  CHRONIC  INDURATIVE  PNEUMONIA     205 

nation.  Bronchiectasis  may  occur  as  a  consequence  of  the  infection 
which  gave  rise  to  the  induration,  but  once  established,  is  likely  to 
lead  to  an  extension  of  the  indurative  process  from  the  retention  of 
infectious  material  within  the  dilated  tubes.  Partial  occlusion  of  the 
bronchi  by  aneurysm,  enlarged  bronchial  lymph  glands,  syphilitic 
ulceration  of  the  bronchi,  newgrowths  or  foreign  bodies  leads  to  infec- 
tion and  indurative  pneumonia  in  parts  supplied  by  the  occluded 
passages.  Atelectasis  may  be  followed  by  induration,  but  the  connec- 
tive tissue  changes  are  here  to  be  ascribed  rather  to  a  complicating 
infection  than  to  this  condition  alone.  Interstitial  changes  occur 
in  the  so-called  brown  induration,  of  chronic  passive  congestion.  The 
syphilitic  pneumonia  of  infants  may  also  lead  to  induration.  Dust 
inhalation  is  of  itself  alone  probably  not  an  adequate  cause  (see 
Pneumonoconiosis) . 

Local  and  circumscribed  induration  may  be  found  at  any  place  in 
the  lung,  but  is  most  frequent  at  the  apices  where  it  is  usually  due  to 
relatively  inactive  or  healed  tuberculosis,  bacterial  invasion  in  connec- 
tion with  the  inhalation  of  dust,  or  to  extension  from  an  inflamed 
pleura.  Among  other  causes  may  be  mentioned  abscess  and  gangrene, 
actinomycosis,  gumma  and  infarction,  and  provided  there  is  also  a 
complicating  infection,  primary  and  secondary  newgrowth,  hydatids, 
foreign  bodies,  and  injuries. 

Pathology. — The  appearances  vary  with  the  cause  and  extent  of  the 
process  and  the  stage  of  development.  Three  principal  forms  may  be 
recognized,  the  massive  or  lobar,  insular  or  bronchopneumonic,  and 
pleurogenous  interstitial  pneumonia. 

1.  Massive  or  Lobar  Form. — The  condition  is  usually  unilateral  and 
involves  the  lower  somewhat  more  often  than  the  upper  lobes.  Bila- 
teral involvement  is  not  infrequent,  or  parts  or  the  whole  of  one  lung 
may  be  affected. 

In  the  early  stages  of  organizing  croupous  pneumonia,  the  affected 
parts  differ  from  ordinary  red  or  gray  hepatization  in  a  less  granular 
or  smooth  section  surface  and  greater  firmness  of  the  tissue  (red  indura- 
tion) .  Later  stages  show  a  change  in  color  from  grayish-red  to  grayish- 
yellow  (yellow  induration),  or  gray  (gray  induration),  a  diminishing 
amount  of  moisture  in  the  cut  surface  and  increasing  toughness  until 
finally  the  lung  is  transformed  into  a  pale  gray  or  slate  colored  (slaty 
induration)  and  contracted  mass  of  scar  tissue,  which  can  be  cut  only 
with  difficulty.  These  various  appearances  may  all  be  present  in  one 
and  the  same  lung.  The  change  in  color  and  the  increasing  firmness 
are  due  to  replacement  of  the  infiltrated  parenchyma  by  connective 
tissue.  Inhaled  pigment  scattered  through  the  lung  may  give  the 
appearance  of  polished  granite,  and  fatty  degeneration  of  the  alveolar 
epithelium  may  impart  dots  of  yellowish  color  to  the  section  surface. 
Microscopic  examination  shows  the  development  of  connective  tissue 
within  the  alveoli  in  the  form  of  plugs  of  tissue  connected  by  means  of 
a  pedicle  with  the  alveolar  wall.    These  plugs  contain  usually  a  net- 


266  •  DISEASES  OF  THE  LUNGS 

work  of  coarse  fibrin  in  the  meshes  of  which  polynuclear  leukocytes, 
round  and  spindle-shaped  cells  are  found.  The  crescentic  interval 
between  the  free  margin  of  the  plug  and  the  alveolar  wall  contains 
swollen  epithelial  cells  and  red  blood  corpuscles.  Bloodvessels  enter 
the  ping  from  the  alveolar  wall  by  way  of  the  pedicle.  Isolated  threads 
or  bundles  of  fibrin  may  be  seen  here  and  there  to  pass  through  the 
alveolar  wall  from  one  to  another  and  neighboring  plugs.  These  com- 
municating fibers  were  first  described  by  Kohn1  and  explained  on  the 
ground  that  there  were  small  openings  in  the  alveolar  wall  through  which 
the  fibers  could  pass,  and  were  regarded  as  the  framework  on  which 
the  connective  tissue  formation  was  built.  Hansemann2  later  showed 
that  the  stomata  are  normally  present  in  the  lung  of  animals.  Organi- 
zation of  the  alveolar  plugs  obliterates  the  alveoli,  and  the  alveolar 
walls  are  thickened  and  infiltrated  with  round  and  later  with  spindle- 
shaped  cells.  The  peribronchial,  perivascular,  interlobular  and  sub- 
pleural  tissue  are  more  or  less  involved.  The  affected  parts  of  the  lung 
are  transformed  into  a  homogeneous,  translucent  connective  tissue  in 
which  it  may  be  difficult  or  impossible  to  recognize  any  remains  of  the 
normal  parenchyma. 

Bronchopneumonia  Form. — Here  also  in  the  more  subacute  or  chronic 
cases  the  alveolar  exudate  becomes  organized,  and  fibrous  tissue  is 
formed  in  the  interalveolar  septa,  the  interlobular,  peribronchial 
and  perivascular  tissue.  The  indurative  process  is  predominantly 
peribronchial,  and  abscess  formation  and  bronchiectasis  are  frequently 
associated  with  it.  The  site  of  the  process  is  very  variable.  The  lower 
lobes  are  more  frequently  affected.  The  condition  may,  however, 
be  confined  to  the  upper  lobes,  or  there  may  be  scattered  foci  through- 
out one  or  both  lungs.  Confluence  of  numerous  bronchopneumonic 
areas  of  induration  may  lead  to  the  involvement  of  an  entire  lobe  or 
the  whole  of  one  lung. 

Pleurogenous  Interstitial  Pneumonia. — This  is  a  well  defined  form. 
Persistent  collapse  of  the  lung  in  consequence  of  an  accumulation 
of  fluid,  air  or  solid  material  in  the  pleural  sac  leads  to  inflammatory 
changes  in  the  lung.  In  typical  instances,  broad  bands  of  grayish- 
white  connective  tissue  extend  from  the  thickened  pleura  by  way  of 
the  interlobular  septa  into  the  lung  tissue.  Infectious  material  travels 
by  way  of  the  lymphatics  from  the  pleura  to  the  lung.  An  opposite 
relation  may  obtain,  and  interstitial  changes  starting  in  the  lung  may 
later  lead  to  involvement  of  the  pleura. 

These  three  forms  represent  the  principal  types  of  the  disease,  but 
are  recognizable  in  only  a  small  proportion  of  the  cases.  In  most 
instances  of  interstitial  pneumonia  which  come  to  postmortem  exami- 
nation, the  onset  appears  to  have  been  insidious  or  too  ill  defined  to 

1  Zur  Histologic  der  indurirenden  fibrinosen  Pneumonie,  Munch,  med.  Woch.,  1893, 
No.  3. 

2  Ueber  die  Poren  der  normalen  Lungenalveolen,  Sitzungsberichte  der  KGL.  Preuss., 
Akad.  d.  Wissenschaften,  1895,  Bd.  xliv,  p.  199. 


SUBACUTE  AND  CHRONIC  INDURATIVE  PNEUMONIA       267 

admit  of  a  definite  statement  concerning  the  method  of  origin.  The 
pathologic  picture  is  complicated  by  the  coexistence  of  old  and  recent 
lesions.  Together  with  the  indurative  changes,  bronchiectasis,  pul- 
monary abscess  and  gangrene  may  be  found.  Acute  bronchopneu- 
monia and  lobar  pneumonia  are  frequent  intercurrent  and  terminal 
events.  Pleuritis  is  practically  a  constant  feature.  Thus  it  is  often 
difficult  to  decide  between  primary  and  secondary  processes. 

Pulmonary  abscesses  appear  to  occur  with  about  equal  frequency 
in  interstitial  pneumonia  secondary  to  bronchopneumonia  and  lobar 
pneumonia.  Bronchiectasis  seldom  complicates  an  indurative  process 
following  unresolved  lobar,  but  is  frequent  after  bronchopneumonia. 

In  the  final  stages  of  an  extensive  induration,  the  affected  lung 
may  be  much  reduced  in  size  and  lie  close  to  the  spine  as  a  firm,  hard, 
airless  mass  which  cuts  with  the  resistance  of  cartilage.  The  section 
surface  is  smooth  and  grayish-white  or  slate  colored.  An  abundance 
of  pigment  may  give  a  blackish  mottling  or  coal-black,  even  coloring 
to  the  tissue.  The  contracted  lung  is  intersected  by  bloodvessels  and 
contains  the  terminations  of  more  or  less  dilated  bronchi.  An  extreme 
degree  of  bronchiectasis  may  exist  and  the  lung  then  be  transformed 
into  a  series  of  cavities.  Ulcerative  degeneration  may  lead  to  the 
development  of  abscess  cavities,  and  if  the  process  has  reached  an 
extreme  grade,  isolated  and  intercommunicating  bronchiectatic  and 
abscess  cavities  may  comprise  the  greater  part  of  the  involved  region 
with  only  little  indurated  tissue  between. 

Microscopic  examination  in  the  less  extensive  involvements  shows 
the  development  of  connective-tissue  about  the  bloodvessels  and  the 
bronchi,  and  between  the  lobules  and  in  the  subpleural  region.  The 
alveolar  walls  are  thickened  and  the  air  spaces  contain  recently  formed 
and  nuclear  connective-tissue  rich  in  bloodvessels  or  older  and  fibrillated 
tissue.  If  the  transformation  is  far  advanced,  it  may  be  impossible 
to  recognize  the  alveoli.  Here  and  there  in  the  midst  of  the  dense 
connective-tissue,  dilated  alveolar  or  infundibular  spaces,  lined  with 
cubical  epithelium  and  resembling  glandular  structures,  may  be 
found. 

Thick  dense  adhesions  may  bind  the  lung  to  the  thoracic  wall, 
and  its  removal  may  be  effected  only  with  the  knife.  In  other  instances, 
and  more  often  when  the  indurative  process  is  of  bronchopneumonic 
origin,  the  pleura  may  be  only  slightly  involved.  The  unaffected  parts 
of  the  same  or  the  other  lung  are  usually  emphysematous.  The  heart 
frequently  shows  hypertrophy  and  dilatation,  affecting  principally 
the  right  ventricle. 

The  necessary  interval  which  must  elapse  between  the  onset  of  the 
infection  and  the  development  of  induration,  probably  varies  within 
wide  limits  in  different  cases.  The  shortest  period  between  the  sudden 
onset  of  pulmonary  trouble  in  patients  previously  free  from  symptoms 
referable  to  the  lung,  and  the  finding  of  an  organizing  pneumonia  at 
postmortem    examination    in    the   Massachusetts    General    Hospital 


268  DISEASES  OF  THE  LUNGS 

series  was  seven  days  in  one  instance.  In  a  second  case  the  interval 
was  nine  days.  Intervals  of  thirteen,  fifteen,  sixteen,  and  seventeen 
days  are  recorded  in  4  other  eases.  According  to  Charcot,1  red  indur- 
ation is  observed  after  an  interval  of  one  month  to  six  weeks,  while 
the  stage  of  gray  induration  may  be  established  after  two  to  three 
months;  and  a  true  fibrous  metamorphosis  is  produced  in  the  space 
of  four  to  five  months,  a  year  or  even  longer. 

Symptoms. — There  is  no  typical  clinical  picture,  and  the  symptoms 
are  usually  due  to  complications  rather  than  to  the  induration  itself. 
In  many  instances,  the  interstitial  change  represents  the  final  result 
of  an  inflammatory  process  which  has  healed,  not  by  resolution,  but 
by  replacement  with  scar  tissue.  If  the  arrest  of  the  disease  is  complete, 
as  it  may  be  in  pulmonary  tuberculosis,  inflammatory  changes  in 
connection  with  dust  inhalation,  in  the  induration  complicating 
pleurisy,  in  the  scarring  of  the  lung  which  takes  place  following  the 
healing  of  unresolved  bronchopneumonia,  abscess  or  gangrene,  gum- 
mata,  infarction  and  other  processes  of  limited  extent,  there  may  then 
be  no  residual  symptoms.  The  involved  region  remains  functionally 
inactive,  but  the  loss  of  a  small  area  of  lung  tissue  is  of  little  moment 
to  the  individual.  On  examination  there  may  be  no  evidence  of  the  indu- 
rative process,  which  may,  however,  be  suspected  from  the  previous 
history,  or  remain  entirely  latent  and  be  first  discovered  at  postmortem 
examination.  Areas  of  small  extent  are  more  likely  to  be  detected 
at  the  apex  than  at  other  places  in  the  lung,  and  may  be  indicated  by 
retraction  of  the  apical  region,  narrowing  of  the  isthmus,  slight 
dulness,  bronchial  breathing,  increase  of  voice,  whisper,  and  tactile 
fremitus.  In  time  these  signs  may  become  less  striking  and  finally 
disappear,  owing  to  the  development  of  emphysema. 

Incompletely  healed  lesions  leading  to  pulmonary  induration  as  an 
incidental  feature  are  accompanied  by  symptoms  which  are  due  prin- 
cipally to  bronchial  catarrh,  bronchiectasis,  abscess,  or  pleurisy. 
The  symptoms  and  physical  signs  in  these  cases  are  those  which  are 
described  in  the  sections  on  these  conditions. 

Finally,  pulmonary  induration  may  be  a  principal  feature  and 
extensive  enough  to  present  characteristic  clinical  aspects.  In  this 
type  the  onset  may  have  been  insidious  or  with  the  symptoms  of  lobar 
pneumonia  or  pleuritis.  The  opportunity  is  occasionally  offered  of 
observing  the  development  of  the  condition.  Thus  induration  may 
follow  recurrent  lobar  pneumonia,  affecting  the  same  pulmonary 
region  and  usually  without  complete  absence  of  pulmonary  infection 
in  the  intervals  between  the  attacks.  Induration  is  more  commonly 
observed  following  a  lobar  pneumonia  of  ordinary  or  severe  course 
in  which  the  fever  continues  elevated  after  its  expected  decline,  or  falls 
by  crisis  or  lysis  only  to  rise  again  after  a  few  days.  The  leukocytosis 
continues,  and  the  rusty  tenacious  sputum  becomes  mucopurulent. 

1  Maladies  des  poumons  et  du  systeme  vasculaire,  1888,  p.  187. 


SUBACUTE  AND  CHRONIC  INDURATIVE  PNEUMONIA     209 

Bleeding  from  fresh  granulation  tissue  may  give  a  bloody  sputum  at 
times.  The  signs  of  solidification  persist,  and  a  continuous  or  remittent 
fever  lasts  for  weeks  or  months,  There  is  loss  of  weight,  strength 
and  appetite,  and  tuberculosis  is  suspected.  A  fatal  result  may  occur 
after  a  variable  interval,  but  it  is  more  common  for  the  fever  gradually 
to  subside,  the  sputum  to  become  less  abundant,  and  the  pulmonary 
signs  to  recede.  The  nutrition  slowly  improves  and  may  again  become 
normal,  but  the  signs  of  localized  trouble  in  the  lung  continue.  With 
the  progress  of  time,  the  signs  become  less  evident  owing  to  contrac- 
tion of  the  affected  region  and  emphysema  of  the  neighboring  parts 
of  the  lung. 

It  is  more  common  to  be  confronted  with  the  interstitial  changes 
already  well  developed.  There  is  then  a  history  of  chronic  cough, 
more  or  less  abundant  sputum,  dyspnea,  and  pain.  The  general  health 
may  or  may  not  be  disturbed,  depending  on  the  degree  of  toxemia 
from  the  persistent  infection.  In  some  cases,  there  is  little  change  in 
the  symptoms  and  physical  signs  over  a  period  of  many  years.  Patients 
with  interstitial  pneumonia,  complicated  by  bronchiectasis  and  single 
or  multiple  pulmonary  abscesses,  are  subject  to  recurring  attacks  of 
bronchial  catarrh.  Extension  of  the  infection  into  neighboring  or 
remote  parts  of  the  lung  is  likely  to  give  rise  to  acute  or  subacute 
bronchopneumonia,  bronchiectasis,  and  pulmonary  abscesses.  An 
elevation  of  temperature  for  a  short  period  is  common.  Coincident 
diminution  in  the  amount  of  sputum  may  suggest  that  a  collection  of 
pus  has  failed  to  find  exit  by  way  of  the  bronchi.  A  chill  may  precede 
such  attacks.  Rapid  subsidence  of  the  fever  may  follow  an  increase 
in  the  amount  of  sputum.  Pleuritis  is  common.  Pneumothorax  is 
rare.  Pulmonary  gangrene  may  occur.  Lobar  pneumonia  is  a  frequent 
terminal  event.  Death  may  also  be  due  to  septicemia,  pyemia, 
malignant  endocarditis,  cerebral  abscess  or  acute  nephritis. 

The  sputum  presents  no  characteristic  features  and  is  due  to  the 
complicating  bronchiectasis,  pulmonary  abscesses,  bronchopneumonia 
or  gangrene.  It  is  absent  in  interstitial  pneumonia  only  when  the  con- 
dition is  uncomplicated  and  the  induration  represents  a  healed  -pul- 
monary lesion.  It  is  of  variable  amount,  mucopurulent  or  purulent, 
oftentimes  of  bad  odor,  and  consists  of  thin  pus  or  thicker  mucopurulent 
masses.  Its  color  is  yellowish  or  greenish.  Admixture  of  coal  dust 
may  give  it  a  blackish  or  coal-black  color.  If  ulceration  of  the  lung 
tissue  is  taking  place,  masses  of  pulmonary  parenchyma  may  be 
found.  Elastic  tissue  may  be  demonstrated  by  appropriate  methods 
of  examination  (see  Pulmonary  Abscess  and  Gangrene).  Microscopic 
examination  shows  pus  cells,  occasional  alveolar  epithelium,  at  times 
containing  pigment  and  various  bacteria. 

Hemoptysis  is  frequent.  Small  amounts  of  blood  may  come  from 
recently  formed  granulation  tissue.  Frank  bleeding  may  be  due  to 
erosion  of  bloodvessels  lining  the  walls  or  traversing  the  lumen  of  pul- 
monary cavities,  or  the  rupture  of  varices  in  the  bronchial  wall.    A 


270  DISEASES  OF  THE  LUNGS 

severe  attack  of  cough  or  sudden  exertion  may  initiate  the  hemorrhage. 
The  amount  of  blood  is  usually  small,  but  large  and  even  fatal  bleeding 
may  occur.  The  bleeding  usually  lasts  several  days,  and  is  commonly 
unaccompanied  by  fever  in  non-tuberculous  cases. 

Physical  Signs. — Single  or  multiple  areas  of  interstitial  pneumonia 
if  small  and  centrally  placed  or  surrounded  by  emphysematous  lung, 
may  give  no  definite  signs  on  examination.  Superficial  areas  are  more 
readily  detected. 

Inspection. — Diminished  expansion  of  the  involved  part  of  the  lung 
is  often  a  striking  feature.  Contraction  of  the  chest  is  frequently  to 
be  noted,  and  is  greater  in  the  more  extensive  unilateral  involvements, 
as  after  unresolved  lobar  pneumonia,  following  bronchostenosis,  and 
with  pulmonary  induration  complicating  empyema.  Thoracic 
deformity  may  reach  its  most  extreme  grade  when  the  interstitial 
process  has  occurred  in  childhood  at  a  period  when  the  chest  is  less 
rigid  than  in  later  life.  If  the  disease  begins  in  adult  life,  contraction 
of  the  lung  may  be  largely  compensated  by  the  displacement  of  internal 
organs  and  with  relatively  little  retraction  of  the  thorax.  Asymmetry 
may  be  accentuated  by  a  considerable  degree  of  emphysema  in  the 
otherwise  unaffected  parts  of  the  lung.  The  shape  of  the  chest  depends 
on  the  site  of  the  process.  Involvement  of  the  apical  region  is  likely 
to  lead  to  marked  depression  of  the  supra-  and  infra-clavicular  fossa? 
and  depression  of  the  cervicohumeral  line  seen  in  profile,  while  involve- 
ment of  the  lower  lobe  leads  to  retraction  of  the  side  and  narrowing  of 
the  intercostal  spaces.  The  diminution  in  size  may  be  confirmed  with 
the  tape.  The  shoulder  on  the  affected  side  droops,  and  there  may  be 
atrophy  of  the  shoulder  girdle,  the  pectorals  and  serrati.  There  is 
frequently  a  variable  degree  of  scoliosis  with  the  convexity  of  the 
spinal  curvature  toward  the  affected  side  and  with  compensatory 
curves  above  and  below. 

Percussion. — The  percussion  note  varies  with  the  site  and  extent  of 
the  process.  Small,  central  areas  may  give  no  change  in  the  note. 
Superficial  areas  must  reach  a  few  centimeters  in  diameter  to  be 
detected  by  percussion.  The  note  is  dull  over  small  and  may  be  flat 
over  large  areas.  If  the  interstitial  process  is  complicated  by  consider- 
able dilatation  of  the  communicating  bronchi  or  a  cavity  in  the  lung, 
the  dull  note  may  have  a  tympanitic,  cracked-pot  or  metallic  quality, 
and  may  change  with  the  mouth  opened  and  closed,  during  inspiration 
and  expiration  and  on  changing  the  position  of  the  patient.  Emphy- 
sema of  the  neighboring  lung  may  obscure  the  findings  on  percussion. 
Hyperresonance  from  emphysema  may  be  noted  in  the  otherwise 
uninvolved  parts  of  the  same  or  the  opposite  lung.  In  consequence 
of  pulmonary  inflation  the  inferior  margin  of  the  opposite  lung  may 
be  abnormally  low  and  change  its  level  relatively  little  during  full 
inspiration,  and  the  sternal  border  may  be  found  by  percussion  to 
project  several  centimeters  beyond  the  median  line  toward  the  affected 
side. 


SUBACUTE  AND  CHRONIC  INDURATIVE  PNEUMONIA        271 

Auscultation. — The  breathing  may  be  feeble  and  vesicular,  broncho- 
vesicular  or  bronchial.  Dilatation  of  the  bronchi  or  cavities  in  the 
lung  may  give  the  breathing  an  amphoric  quality.  Rales  of  a  con- 
sonating  or  non-consonating  quality,  and  fine,  medium  or  coarse,  are 
practically  constantly  present  in  cases  complicated  by  bronchitis, 
bronchiectasis  or  cavities  in  the  lung.  They  may  be  present  in  mild 
cases  only  in  the  morning  before  the  accumulated  excretion  is  expelled. 
In  patients  with  small  and  circumscribed  or  scattered  areas,  centrally 
placed,  persistent  rales  over  the  involved  regions  may  be  the  only 
finding  on  physical  examination.  An  increased  loudness  of  the  cardiac 
sounds  may  frequently  be  observed  over  areas  of  interstitial  pneu- 
monia, especially  when  the  left  upper  lobe  is  involved.  Increase  in 
the  intensity  of  the  voice  and  whisper  may  be  found  over  the  consoli- 
dated areas.  Loud  vesicular  breathing  with  some  prolongation  of 
expiration  may  be  heard  over  uninvolved  or  emphysematous  parts  of 
the  lung. 

Palpation. — Diminished  respiratory  motion,  and  narrowing  of  the 
intercostal  spaces  may  be  confirmed  by  palpation.  An  increase  in 
tactile  fremitus  is  observed  over  infiltrated  areas  of  sufficient  extent 
provided  unobstructed  bronchi  communicate  freely  with  the  involved 
region. 

Displacement  of  the  Viscera. — The  heart  may  be  greatly  displaced 
toward  the  affected  side.  When  the  cirrhotic  process  affects  the  left 
lung,  and  especially  with  retraction  of  the  left  upper  lobe,  there  is 
likely  to  be  visible  pulsation  in  the  parasternal  region  in  the  second, 
third,  and  fourth  interspaces.  The  apex  beat  may  be  seen  and  felt 
a  considerable  distance  beyond  its  normal  position  toward  the  left 
axilla.  Careful  outlining  of  the  heart  by  percussion  will  be  of  assistance 
in  deciding  between  displacement  and  enlargement.  With  right- 
sided  pulmonary  processes  the  displacement  may  be  far  to  the  right 
and  congenital  dextrocardia  may  be  suspected.  In  extreme  degrees 
of  pulmonary  cirrhosis,  it  may  be  difficult  or  impossible  to  be  sure  of 
the  position  of  the  heart.  Systolic  murmurs  are  not  infrequently 
heard  over  displaced  hearts,  and  are  probably  due  to  dislocation  or 
compression  of  the  pulmonary  artery. 

As  a  result  of  pulmonary  contraction,  the  diaphragm  may  be  drawn 
upward  far  beyond  its  normal  position  on  the  involved  side,  as  can  be 
demonstrated  by  .T-ray  examination.  An  appreciation  of  this  is  of 
especial  importance  in  cases  of  pulmonary  induration  complicated 
by  pleurisy  with  effusion,  pulmonary  abscess  or  gangrene  in  which 
surgical  exploration  is  contemplated.  It  is  always  well  to  determine 
the  position  of  the  diaphragm  by  means  of  the  .r-rays  before  interfer- 
ence is  attempted. 

Elevation  of  the  diaphragm  on  the  left  side  elongates  the  area  of 
tympany  from  the  stomach  and  intestines  over  Traube's  semilunar 
space,  and  a  tympanitic  percussion  note  may  be  obtained  upward  as 
far  as  the  fifth  rib  or  higher. 


272  DISEASES  OF  THE  LUNGS 

Clubbing  of  the  fingers  is  frequently  observed  in  cases  with  inter- 
stitial pneumonia  complicated  with  pulmonary  suppuration.  From 
four  to  six  months  is  usually  necessary  for  the  development  of  the 
changes  in  the  ringers. 

Diagnosis. — It  is  often  impossible  to  obtain  definite  signs  from 
limited  areas  of  pulmonary  induration  even  when  situated  at  the 
periphery  of  the  lung.  Numerous  scattered  foci  centrally  placed  may 
also  readily  escape  detection.  With  long  standing  cough  and  expec- 
toration, signs  of  pulmonary  solidification  and  contraction  of  the  chest 
or  displacement  of  the  viscera,  the  diagnosis  may  be  made.  Post- 
mortem examination  of  patients  long  subject  to  pulmonary  infection 
seldom  fails  to  disclose  an  increase  in  connective-tissue  as  an  incidental 
or  principal  lesion,  and  the  condition  may  therefore  be  regarded  as 
probable,  even  if  its  exact  site  cannot  be  determined,  in  those  who  have 
suffered  from  the  expectoration  of  purulent  sputum  for  weeks  or 
months.  The  site  of  the  process  may  be  suggested  by  the  finding  on 
repeated  examinations  of  rales  persistently  localized  at  one  or  more 
places.     The  determination  of  the  cause  is  often  difficult. 

An  origin  in  lobar  pneumonia,  though  uncommon,  is  suggested  when, 
preceding  the  evidences  of  induration,  there  is  a  history  of  single  or 
recurring  attacks  of  acute  illness  of  sudden  onset,  with  chill,  rapid 
rise  of  fever,  cough  with  rusty  sputum  and  pain  in  the  side,  lasting 
about  a  week  and  ending  by  crisis  or  lysis.  Great  caution  must  be 
observed,  however,  to  exclude  pulmonary  abscess,  empyema  and  tuber- 
culosis which  are  much  more  common  causes  of  an  apparent  delay  in 
resolution  than  indurative  pneumonia.  A  confusion  between  empyema 
and  indurative  pneumonia  is  the  most  common  error.  Collections  of 
pus  between  the  lobes  of  the  lung  or  between  the  diaphragm  and  the 
base  of  the  lung  are  to  be  considered  as  well  as  the  more  common 
accumulations  between  lung  and  chest  wall.  Sacculated  exudates,  inter- 
posed little  or  not  at  all  between  lung  and  chest  wall,  are  most  diffi- 
cult of  differentiation,  and  owing  to  the  retraction  of  the  neighboring 
lung,  may  exhibit  typical  signs  of  pulmonary  solidification,  with  dulness, 
loud  bronchial  breathing,  and  increase  of  voice  and  whisper.  A  pecu- 
liar regophonic  quality  to  the  voice,  marked  diminution  or  absence  of 
the  tactile  fremitus  and  an  abnormal  degree  of  dulness  or  even  flat- 
ness on  percussion  are  suggestive  of  pleural  effusion.  Pleural  exudates 
which  are  situated  in  the  paravertebral  region  give  dulness  along  the 
edge  of  the  spinal  column,  a  region  usually  resonant  in  uncomplicated 
pneumonia.  More  extensive  exudates  may  so  far  exceed  the  limits 
of  the  pulmonary  boundary  as  to  cause  dulness  in  the  opposite  para- 
vertebral region  (Grocco's  paravertebral  triangle.).  Dislocation  of 
the  heart  is  a  valuable  differential  sign.  With  uncomplicated  pulmon- 
ary induration,  contraction  of  the  affected  region  dislocates  the  heart 
toward  the  affected  side,  while  accumulations  of  pleural  fluid  tend  to 
dislodge  the  heart  in  the  opposite  direction.  A  persistent  leukocytosis 
suggests  pus.    In  doubtful  cases,  examination  by  means  of  the  .T-rays 


SUBACUTE  AND  CHRONIC  INDURATIVE  PNEUMONIA        273 

and  exploratory  puncture  must  be  used.  Exploratory  puncture  should 
not  be  done  unless  the  position  of  the  diaphragm  is  known,  and  this 
can  best  be  determined  by  x-ray  examination. 

Of  the  different  forms  of  pleurisy,  it  is  especially  the  purulent 
variety  which  is  likely  to  lead  to  interstitial  pneumonia.  In  cases  in 
which  pleurisy  is  a  cause,  there  is  likely  to  be  a  history  at  onset  of 
pain  aggravated  by  cough  and  long  breath,  and  symptoms  of  sepsis 
are  a  prominent  feature.  There  may  be  a  scar  of  operation  or  the 
history  of  the  withdrawal  of  pus.  A  neglected  empyema  may  rupture 
into  the  lung  and  a  large  amount  of  pus  be  expectorated  at  one  time. 
Such  obvious  perforation  is  less  common  than  the  slow  invasion  of  the 
lung  with  multiple  areas  of  suppuration  and  induration  and  the  expec- 
toration of  small  amounts  of  purulent  sputum  at  frequent  intervals. 
Owing  to  the  frequency  with  which  pleurisy  complicates  interstitial 
pneumonia,  some  care  must  be  taken  in  deciding  from  the  patient's 
story  alone  whether  the  pleurisy  is  primary  or  secondary.  An  apical 
site  of  the  indurative  process  is  against  purulent  pleurisy  as  a  cause, 
but  sacculated  empyema  over  an  upper  lobe  occurs  in  rare  instances. 

An  origin  in  bronchopneumonia  may  be  suspected  when  an  indura- 
tive process  occurs  after  a  primary  pneumonia  in  children  under  two 
years,  since  at  this  period  bronchopneumonia  is  the  more  common 
type.  Bronchopneumonia  may  also  be  suspected  as  a  cause  when  the 
condition  follows  measles,  whooping  cough  and  diphtheria,  bronchitis, 
the  extension  of  an  infection  from  the  pleura  or  abdomen,  obstruction 
of  the  bronchi  by  new  growths  within  or  compression  from  without, 
the  aspiration  of  foreign  bodies  or  inhalation  of  food,  drink  or  septic 
material.  Induration  complicating  abscess  or  gangrene  is  usually  due 
to  bronchopneumonia  which  arises  by  extension  or  the  inhalation  of 
septic  material  into  nearby  or  remote  parts  of  the  lung. 

In  the  determination  of  the  cause,  tuberculosis  is  always  to  be  con- 
sidered, and  its  exclusion  is  often  difficult  and  at  times  impossible. 
Certain  factors  of  importance  in  the  differentiation  between  the  more 
chronic  types  of  tuberculous  and  non-tuberculous  pulmonary  infection 
are  discussed  under  the  diagnosis  of  bronchopneumonia,  and  need  not 
be  repeated.  An  apparent  lobar  pneumonia  which  terminates  in  tuber- 
culosis is  usually  tuberculous  from  its  inception,  but  tuberculosis  may 
be  engrafted  on  non-tuberculous  induration.  A  certain  proportion 
of  the  cases  of  pleurogenous  interstitial  pneumonia  are  tuberculous, 
but  purulent  pleurisy  is  less  commonly  due  to  the  tubercle  bacillus  than 
the  primary  fibrinous  and  serofibrinous  forms.  The  absence  of  tubercle 
bacilli  from  the  sputum  is  of  less  moment  in  cases  with  interstitial 
pneumonia  than  in  the  more  acute  pulmonary  processes,  since  an 
abundant  development  of  scar  tissue  may  wall  off  the  tuberculous 
foci  and  prevent  expectoration  of  bacilli.  A  final  decision  against 
tuberculosis  may  not  be  possible  until  tuberculin  has  been  given 
and  the  tests  have  proved  negative  in  increasing  doses  up  to  and 
including  10  mg. 
18 


274  DISEASES  OF  THE  LUNGS 

In  cases  of  indurative  pneumonia  not  otherwise  to  be  explained, 
bronchostenosis  is  to  be  considered.  A  foreign  body,  syphilitic  ulcera- 
tion and  new  growth  arising  from  the  bronchial  wall  and  compression 
from  without  of  aneurysm,  tumor  or  enlarged  glands  are  possible  causes. 
More  marked  dyspnea  than  can  be  explained  by  the  physical  findings, 
attacks  of  suffocation,  stridor,  diminished  or  absent  respiratory  motion 
and  breathing,  and  sibilant  or  sonorous  rales  over  the  site  of  the 
obstructed  bronchus  may  be  suggestive.  There  may  be  little  or  nothing 
of  moment  in  the  history,  and  physical  examination  may  offer  no 
additional  evidence.  In  some  cases,  however,  a  foreign  body  may  be 
known  to  have  been  inhaled.  A  history  of  syphilis  may  be  obtained,  or 
late  lesions  of  this  disease  may  be  present  elsewhere.  Tracheoscopic 
examination  may  reveal  ulcerations,  or  the  Wassermann  test  may  be 
positive.  New  growths  of  small  size  arising  from  the  bronchial  wall 
and  without  metastases  and  isolated  enlargement  of  the  bronchial 
glands  can  hardly  be  diagnosed  unless  some  indication  of  their  presence 
is  found  on  .T-ray  examination.  Malignant  disease  of  the  mediastinum 
or  aneurysm  may  be  detected  after  a  careful  history,  and  physical 
examination  aided  by  the  .T-rays. 

In  some  instances,  tumor  of  the  pleura  or  the  lung  may  simulate 
pulmonary  induration  from  the  signs  of  pulmonary  solidification  and 
contraction  of  the  side.  Stridor,  inequality  of  the  pupils  or  the  pulses, 
enlargement  of  the  cervical  or  axillary  glands,  dilatation  of  the  super- 
ficial veins  of  the  thorax,  dulness  over  the  anterior  or  posterior  medi- 
astinum, and  recurrent  laryngeal  paralysis  may  be  suggestive. 

Actinomycosis  of  the  lung  and  pleura  is  to  be  considered  in  the  pres- 
ence of  pulmonary  induration,  and  may  occur  as  a  primary  or  secondary 
infection.  The  tendency  of  the  infection  to  extend  to  the  soft  parts  of 
the  thorax  is  a  striking  and  characteristic  feature,  but  in  the  early 
stages  there  are  likely  to  be  no  outward  manifestations,  and  the  diag- 
nosis can  be  made  only  by  finding  actinomyces  in  the  sputum. 

Prognosis. — The  outlook  depends  on  the  cause  of  the  induration 
and  the  complications.  Actinomycotic  and  aspiration  pneumonia  are 
very  fatal  forms.  Unresolved  lobar  pneumonia  may  last  for  weeks 
or  months,  and  finally  end  in  functional  efficiency  of  the  lung  and 
the  gradual  disappearance  of  physical  signs.  In  individual  cases,  the 
patient's  chances  must  be  estimated  by  the  severity  of  the  infection 
and  the  general  condition.  The  prospects  of  complete  recovery  are 
less  good  w7hen  the  induration  follows  bronchopneumonia,  because  of 
the  damage  to  the  bronchial  wall.  In  all  types  of  the  disease,  the 
induration  itself  may  represent  a  slowly  progressive  lesion  in  which 
the  defensive  action  of  the  body  is  inadequate  to  repel  the  progress 
of  the  infection,  or  a  more  or  less  complete  cure.  Unfortunately  in 
many  cases,  though  the  patient  survives,  the  infection  lurks  persist- 
ently in  dilated  bronchi  or  pulmonary  cavities.  Dyspnea,  cough,  and 
expectoration  then  continue.  Recurrent  bronchopneumonia  is  common 
and  is  followed  by  extension  of  the  indurative  process.    In  tuberculosis 


SUBACUTE  AND  CHRONIC  INDURATIVE  PNEUMONIA       275 

the  indurative  process  is  conservative,  and  complete  encapsulation 
of  caseous  masses  may  effect  an  arrest  of  the  disease.  Death. may 
occur  from  hemoptysis  or  from  gradual  failure  of  the  right  heart. 
In  cases  of  fibroid  induration  due  to  tuberculosis,  amyloid  may  be 
partly  responsible  for  a  fatal  termination. 

Prophylaxis. — Preventive  measures  must  be  directed  against  the 
causes  of  pulmonary  induration.  The  avoidance  of  dust,  the  preven- 
tion of  tuberculosis,  syphilis,  actinomycosis,  aspiration  and  broncho- 
pneumonia and  pleurisy,  and  the  early  removal  of  foreign  bodies  from 
the  bronchi  are  some  of  the  problems.  Care  in  the  treatment  of  existing 
pulmonary  or  pleural  disease  is  important.  Improvement  of  the  general 
nutrition,  rest  in  bed  while  there  is  fever,  avoidance  of  exposure  to 
cold  and  draughts  when  overheated  or  insufficiently  clad,  the  early 
and  complete  drainage  of  empyema,  and  the  evacuation  of  pulmonary 
abscesses  in  properly  selected  cases  may  prevent  the  development  or 
extension  of  induration. 

Treatment. — Little  or  nothing  can  or  need  be  done  for  pulmonary 
induration  which  represents  a  healed  lesion  of  the  lung  without 
complications.  In  cases  in  which  an  infection  persists  with  cough  and 
expectoration,  such  general  measures  as  are  applicable  to  tuberculous 
patients  should  be  advised.  An  occupation  or  life  in  the  open  air, 
in  an  atmosphere  free  from  dust  and  in  an  equable  temperature  is 
desirable.  An  improvement  of  the  nutrition  by  an  abundance  of  food, 
fresh  air  and  rest  should  be  sought  in  patients  whose  general  condition 
is  below  par.  A  cool  morning  bath  or  shower,  followed  by  a  hard  rub 
with  a  coarse  towel,  may  assist  in  improving  the  general  tone.  For 
patients  with  means  and  inclination  for  travel,  the  winters  may  be 
spent  in  the  South. 

In  non-tuberculous  cases,  with  little  or  no  persistent  infection  and 
with  developing  or  established  contraction  of  the  side,  pulmonary  gym- 
nastics may  be  recommended.  In  tuberculous  lesions,  such  exercises 
are  contra-indicated  for  fear  of  aggravating  an  active  lesion  or  exciting 
a  slumbering  process  to  activity.  In  suitable  cases,  deep  inspiration 
and  expiration  for  a  number  of  times  in  the  morning  and  afternoon 
may  first  be  tried.  More  vigorous  exercises  may  be  added.  Thus  the 
patient,  standing  upright  and  lightly  clad,  may  .raise  the  arm  on  the 
affected  side,  laterally,  through  the  horizontal  to  the  vertical  position 
at  the  side  of  the  head.  Deep  inspiration  may  accompany  this  motion. 
With  both  arms  outstretched  in  the  lateral  position,  lateral  bending 
of  the  trunk  away  from  the  affected  side  or  torsion  of  the  trunk  with 
the  pelvis  fixed,  may  be  practiced.  Various  simple  exercises  may  also 
be  prescribed  with  dumb-bells  or  pulley-weights.  In  regulating  the 
daily  life  of  patients  with  pulmonary  induration,  attention  must  be 
paid  to  the  condition  of  the  heart  and,  mindful  of  the  strain  which 
an  impeded  pulmonary  circuit  puts  on  the  right  ventricle,  caution 
should  be  suggested  against  overexertion. 


CHAPTER  XV. 
PNEUMONOCONIOSIS. 

This  term  (from  xueufjuou  lung  and  $  xbvtc,  the  dust)  was  applied 
by  Zenker1  to  a  condition  arising  in  consequence  of  the  inhalation  of 
dust.  Since  the  changes  formerly  ascribed  to  dust  are  probably  in 
large  part,  if  not  entirely,  due  to  bacteria,  the  subject  would  not 
deserve  separate  consideration  were  it  not  that  dust  undoubtedly 
disposes  to  pulmonary  disease. 

Historical  Note. — Different  views  have  been  held  concerning  the 
nature  and  source  of  pulmonary  pigment  in  normal  and  pathologic 
conditions  of  the  lung. 

Origin  from  Without  of  Pigment  in  the  Lung. — In  1703,  Ramazzini2 
stated  that  certain  stone  cutters  became  asthmatic  and  phthisical 
from  the  inhalation  of  pointed  and  angular  fragments  of  stone. 

Pearson3  first  suggested  that  black  pigmentation  of  the  lung  and 
bronchial  glands  was  due  to  the  inhalation  of  carbon  and  soot. 
Laennec4  made  a  distinction  between  the  constant  black  mottling  of 
the  normal  lung,  the  matiere  noire  pulmonaire,  and  melanosis,  suggest- 
ing that  the  black  color  may  in  part  come  from  the  smoke  of  lamps 
and  combustible  bodies.  This  simple  explanation  did  not  go  unchal- 
lenged. Virchow5  denied  it  and  maintained  that  the  so-called  normal 
pigmentation  was  due  to  extravasated  blood  pigment. 

Gregory6  was  the  first  to  publish  a  case  of  pathologic  pigmentation, 
and  additional  evidence  through  the  publications  of  Erdmann,7 
Thompson,8  Marshall,9  Graham,10  Hamilton,11  Gibson,12  Andral,13 
Rilliet,14  Stratton,15  who  proposed  the  name  anthracosis,  and  Brock- 
mann16  indicated  that  this  pigmentation  occurred  to  a  much  greater 
degree  in  occupations  in  which  the  workers  were  exposed  to  an 
atmosphere  rich  in  carbon  particles,  as  in  coal  miners,  or  in  persons 
otherwise  exposed  to  coal  dust.  Christison  (in  Gregory's  case), 
Graham  and  Lecanu  (in  Rilliet's  case)  confirmed  Pearson's  observa- 
tion on  the  identity  of  the  substance  with  carbon. 

i  Deut.  Arch.  f.  klin.  Med.,  1866-67,  vol.  ii. 

2  De  morbis  artificum  diatribe  Ultrojesti,  1703. 

3  Philosophical  Transactions,  1813,  ii,  159. 

4  Traite  de  l'auscultation  mediate,  1813,  2d  ed.,  Paris,  1826,  T.  ii,  p.  34. 

6  Virchow's  Arch.,  1847,  Bd.  i. 

-*  Edinburgh  Med.  and  Surg.  Jour.,  1831,  xxxvi,  389. 

7  Hufeland  and  Osann,  Jour.  f.  prakt.  Heilkinde,  December,  1831,  p.  4. 

8  Medicochirurgical  Trans.,  1857,  xx,  230,  and  1838,  xxi,  340. 

»  Lancet,  May  17,  1834.  «  Edinburgh  Med.  and  Surg.  Jour.,  1834,  xlii,  323. 

11  Ibid.,  p.  297.  «  Lancet,  1834. 

13  Laennec,  Traite  de  l'auscultation  mediate,  1837,  4th  ed.,  pp.  258  and  501,  PI.  B. 
M  Arch.  gen.  de  med.,  June,  1838,  p.  160. 
15  Edinburgh  Med.  and  Surg.  Jour. ,  133|8 ,  xlix. 

1S  Hannov.  Annalen  f.  d.  ges.  Heilk.,  Jahrg.,  1844,  N.  F.  iv,  and  Die  metallurg.  Krank- 
heiten  des  Obcrharzes,  1851,  p.  116. 


PNEUMONOCONIOSIS  277 

The  inhalation  of  carbon  was  accepted  as  a  cause  of  the  condition  in 
England,  but  this  explanation  was  contested  in  Germany,  and  especially 
by  Virchow,  on  the  ground  that  if  the  pigment  came  from  without, 
its  presence  in  the  lung  itself  between  the  elastic  fibers  and  in  the 
connective  tissue  must  be  ascribed  to  the  penetration  of  solid  particles 
through  sound  mucous  membranes,  and  the  possibility  of  such  an 
invasion  he  was  not  disposed  to  accept.  Then,  too,  not  all  coal 
miners  were  affected  with  the  disease,  and  in  two  instances,  reported 
by  Barthelmess1  and  Begbie,2  an  outspoken  melanosis  was  observed 
in  persons  unexposed  to  the  inhalation  of  coal  dust.  Virchow3 
regarded  the  rare  presence  of  the  pigment  in  the  alveolar  wall  and 
its  more  common  position  in  the  interlobular  and  subpleural  con- 
nective tissue  as  against  the  inhalation  theory.  He  also  emphasized 
the  lack  of  resemblance  between  the  black  granules  in  the  lung  and 
the  rather  brown  than  black  particles  of  carbon  and  soot.  He 
regarded  the  pigmentation  of  the  "miner's  lung"  like  the  pigmenta- 
tion of  the  normal  lung,  as  due  to  great  respiratory  efforts  of  the 
workers  and  the  consequent  catarrh  and  extravasation  of  blood. 

An  important  step  in  establishing  the  inhalation  theory  was  made 
by  Traube4  who  found  small  black  particles,  some  of  which  showed 
one  or  several  regularly  circular  openings  in  their  centres  or  semi- 
circular defects  of  varying  size  at  the  margin,  in  the  sputum  of  a  patient 
who  had  handled  charcoal  for  about  twelve  years.  Traube  recognized 
these  as  inhaled  charcoal  particles,  and  examination  of  the  dust  in 
the  place  where  the  patient  had  worked,  showed  similar  particles. 
At  autopsy,  the  cut  surface  of  the  lung  was  a  homogeneous  black 
color.  On  pressure,  a  black  ink-like  fluid  could  be  expressed.  No  trace 
of  new-formed  connective  tissue  or  tuberculosis  could  be  demon- 
strated. In  the  sputum  and  in  the  lung  were  large  cells  resembling 
alveolar  epithelium,  containing  black,  angular  particles.  No  micro- 
scopic examination  of  the  lung  ,was  made,  but  in  a  later  case  reported 
by  Traube,5  Cohnheim  found  carbon  particles  in  the  alveolar  epithe- 
lium, in  the  interstitial  tissue  in  places  in  such  abundance  as  to  sur- 
round the  alveoli  like  black  rings,  and  in  the  bronchial  glands. 
Nowhere,  however,  was  the  interstitial  tissue  increased  in  amount. 
An  accompanying  ulcerative  process  was  due  to  tuberculosis  Traube's 
observations,  together  with  cases  reported  by  Maurice,6  Kuborn,7 
Villaret,8  Crocq,9  and  others  established  the  origin  from  without  of 
pigmented  particles,  and  the  invasion,  not  only  of  the  lung,  but  also 
the  bronchial  glands. 

Zenker's10  report  of  a  case  of  siderosis  pulmonum  established  the 
invasion  of  the  lung  by  metallic  dust.  In  this  case,  the  patient,  a 
woman,   aged  thirty-one  years,  had  worked  for  seven  years  in  a 

1  Diagnose  der  Lungennielanose,  Erlangen,  Inaug.  Diss.,  Abh.,  1S55. 

2  Monthly  Journal.  s  Edinburgh  Med.  Jour.,  September,  1858,  iv,  204. 
.    4  Deut.  Klin.,  1860,  Nos.  49  and  50.  5  Berl.  klin.  Woch.,  1866,  No.  3. 

6  Gaz.  med.  de  Paris,  1862,  vol.  vii.  7  Presse  med.,  1862,  p.  27. 

8  Cas  rares  d'anthracosis,  Paris,  1862.  9  Presse  med.,  1862,  pp.  37-44. 

10  Deut.  Arch.  f.  klin.  Med.,  1866-67,  vol.  ii. 


278  DISEASES  OP  THE  LUNGS 

small,  unventilated  room,  preparing  blotting  paper  for  small  books, 
between  the  leaves  of  which  Hue  leaf  gold  was  placed.    The  blotting 

paper  was  impregnated  with  finely  pulverized  English  red  and  the 
atmosphere  of  the  room  was  filled  with  dust.  At  autopsy,  the  exterior 
and  section  surface  of  the  lung  showed  an  intense  brick-red  color. 
Several  large  cavities  and  numerous  firm,  fibrinous  nodules  were 
scattered  through  both  lungs.  The  two  lungs  weighed  1500  grams 
and  contained  about  21  to  22  grams  of  oxide  of  iron.  Four  girls 
worked  in  the  room.  Of  the  others,  none  complained  of  pulmonary 
symptoms.  One  had  "colored"  for  ten  years  and  her  respiratory 
organs  were  sound. 

Zenker  proposed  the  name  siderosis  puhnonum  (from  aidypo;;  iron) 
for  this,  and  for  the  whole  group  pneumonoconiosis. 

^  irchow,1  influenced  by  such  reports  and  having  convinced  himself 
that  the  soot  particles  from  the  miner's  lamp  could  not  be  distinguished 
microscopically  from  the  black-pigment  granules  in  the  lung,  relin- 
quished his  earlier  opinion  and  accepted  the  existence  of  a  true 
pulmonary  anthracosis. 

The  Intestinal  Theory. — Yillaret's2  opinion  that  inhaled  dust  particles, 
especially  carbon,  were  swallowed  and  reached  the  lungs  indirectly 
after  absorption  from  the  stomach  and  intestines,  has  recently  been 
supported  by  Vansteenberghe  and  Grysez.3  Arnold's4  classical  studies, 
however,  showed  that  while  following  inhalation  experiments  in 
animals,  carbon  particles  were  constantly  found  in  the  lumen  of  the 
intestines,  they  were  not  found  in  the  intestinal  wall,  the  chyle  vessels 
or  the  mesenteric  glands.  The  experiments  of  Aschoff',5  Schultze,6 
Cohn,7  and  Beitzke8  show  that  foreign  particles  injected  into  the 
abdominal  cavity  are  distributed  by  way  of  the  lymph  stream  and 
the  thoracic  duct  to  the  circulating  blood  and  lodge  principally  in  the 
spleen,  liver,  and  bone  marrow\  It  is  well  recognized  that  spontaneous 
pulmonary  anthracosis  is  not  uncommon  among  adult  animals,  and 
it  is  evident  that  the  aspiration  of  foreign  particles  may  take  place 
while  animals  are  being  fed  with  a  tube.  Schultze  and  Beitzke 
failed  to  find  anthracosis  in  animals  fed  through  a  gastric  fistula. 
In  Beitzke's  experiment,  an  animal  allowed  to  inhale  soot  after 
occlusion  of  a  principal  bronchus  showed  soot  only  in  those  parts  of 
the  lung  not  supplied  by  the  occluded  bronchus.  The  evidence  is 
therefore,  strongly  against  an  intestinal  origin. 

1  Virchow's  Arch.,  1866,  xxxv,  186. 

2  Cas  rare  d'anthracosis  suivi  de  quelques  considerations  physiologiques  et  patho- 
logiques,  Paris,  1862. 

3  Sur  l'origine  intestinal  de  i'anthracose  pulmonaire,  Annal,  Past.,  1905,  Bd.  xix, 
p.  787. 

A  1'ntersuchungen  fiber  Staubinhalation  und  Staubmetastase,  Leipzig,  1885. 

5  Experimentelle  Untersuchungen  liber  Russinhalationen  bei  Tieren,  Beitr.  z.  Klinik 
d.  Tuberkulose,  Bd.  vi,  H.  2,  p.  147. 

6  Gibt  es  einen  intestinalen  Ursprung  der  Lungenanthrako.se?  Munch,  med.  Woch., 
1906,  No.  35,  p.  1702. 

7  Die  Lungenanthrakose  und  ihre  Entstehung  vom  Darni  aus.,  Bcrl.  klin.  Woch., 
1906,  No.  14,  p.  1429. 

8  Leber  den  Ursprung  der  Lungenanthrakose,  Virchow's  Arch.,  1907,  clxxxvii,  183. 


PNBUMONOCONJOSJH  270 

Etiology. — Relation  Between  Dust  and  Pulmonary  Disease.  As 
dust  is  a  normal  and  necessary  constituent  of  the  atmosphere,  without 
which  there  would  be  no  rain,  fog  or  clouds,  it  is  inhaled  by  everyone 
in  varying  amounts.  The  amount  of  dust  is  greater  in  thickly  settled 
regions  and  in  certain  occupations.  Under  healthy  conditions  most 
of  the  inhaled  particles  are  caught  in  the  upper  parts  of  the  respiratory 
tract  and  swept  outward  by  the  ciliated  epithelium.  The  normal 
defenses  of  the  body,  however,  are  insufficient  to  protect  those  con- 
stantly exposed  to  an  atmosphere  heavily  laden  with  dust,  as  is  shown 
by  the  constant  presence  of  coal  dust  at  autopsy  in  the  lungs  of  adults 
who  have  lived  in  the  city. 

It  has  long  been  recognized,  however,  that  workers  in  factories 
and  trades  where  the  atmosphere  is  heavily  laden  with  dust,  more 
often  suffer  from  diseases  of  the  respiratory  tract  than  others  not  so 
exposed.  According  to  the  statistics  of  Weyl,1  among  292,536  persons 
receiving  insurance  for  illness  (1896-1899),  there  were  82,101  instances 
of  disease  of  the  respiratory  organs,  including  38,926  cases  of  pulmonary 
tuberculosis.  Thus,  of  the  whole  number,  about  28  out  of  every  100 
patients  suffered  from  disease  of  the  respiratory  tract,  and  about  13 
of  these  from  pulmonary  tuberculosis.  According  to  the  United 
States  Census  Report  for  1900,  consumption  caused  14.5  per  cent, 
of  all  deaths  for  all  occupied  males.  With  these  statistics  for  com- 
parison, the  incidence  of  respiratory  disease  and  of  phthisis  among 
workers  in  dusty  occupations  may  be  noted. 

Hirt2  finds  that  out  of  every  100  patients  among  workers  in  dusty 
occupations,  of  those  inhaling  mineral  dust  about  51  suffered  from 
respiratory  disease  and  about  25  of  these  from  phthisis;  of  those 
inhaling  vegetable  dust  about  46  suffered  from  respiratory  disease  and 
about  13  of  these  from  phthisis;  of  those  inhaling  animal  dust  about 
44  suffered  from  respiratory  disease  and  about  20  of  these  from 
phthisis;  of  those  inhaling  metal  dust  about  43  suffered  from 
respiratory  disease  and  about  28  of  these  from  phthisis. 

Later  figures,  as  those  given  by  Sommerfeld,3  likewise  indicate  that 
tuberculosis  is  more  common  among  workers  in  dust. 

Deaths  from  Mortality 

tuberculosis  from  tuber- 

among  1000  losis  in  1000 
living .  deaths. 

Occupations  without  dust 2 .  39  381 . 0 

Occupations  with  dust 5.42  480.0 

Average 5.16  478.9 

Corresponding  male  population  in  Berlin    .      .      .      .4.93  332 . 3 
Occupations  with  the  development  of 

A.  Metallic  dust 5.84  470.6 

1.  Copper  trades 5.31  520.5 

2.  Iron  trades 5 .  55  403 . 7 

3.  Lead  trades 7.79  501.7 

B.  Mineral  dust 4.42  403.4 

C.  Organic  dust 5.64  537.04 

1  Handbuch  der  Arbeiter  Krankheiten,  1908,  p.  39. 

2  Die  Krankheiten  der  Arbeiter,  Erster  Theil,  Die  Staubs-inhalations-Krankheiten, 
1875,  p.  1. 

3  Handbuch  der  Gewerbekrankheiten,   1898,  p.  344. 


280 


DISEASES  OF  THE  IJXCS 


The  statistics  hearing  on  occupation  and  mortality  from  consumption 

compiled  by  Miss  Lillian  Brandt,  from  the  United  States  Census 

Report  for  1900,  and  graphically  shown  in  the  accompanying  diagram 

are  reproduced  from  the  Handbook  on  the  Prevention  of  Tuberculosis 

and   show   in   greater  detail   the  death  rate  from   consumption   in 

fifty-three  specific  employments  or  small  groups  of  employment  more 

or  less  alike: 

Fig.  38 


►   8" 


list 


|  Marble  and  stone  cuttcrs(IV) 


■■   PlutOTfl 

|  Compositon 
I  Servants (I) 


and  whitewashes  (IV) 
printers,  and  pressman  (IV) 


■  Hat  and  cap  uiakers(IV) 
Bookkeepers,  clerk: 


and  copyists(II) 


■  Laborers  (not  agriculturalKD 
|  Tinners  and  tinware  makers  (IV) 


■  Cabin 

|  "Mu.-i''ia 


:  makers  and  upholsterers  (IV) 
i  and  teachers  of  music  (VI) 


|  Glass  blowers  and  glass  workers  (IV) 

s(V) 


B  Sailors,  pilots,    fishermen, 
I  Painters,  glaziers,  and  varni: 


Leather  makers (IV) 
Apothecaries,  pharmacists,  etc. (VII) 
Coopers  (IV) 

(IV) 


Masons  (brick  andstonc)(IV) 
Butchers  (IV) 
Saloon  keepers,  liquor  dealers,  bartenders,  restaurant  keeperstVIII) 


1  Livery  stable  keepers  and  hostlers  (VIII) 
Draymen,  hackmen,  teamsters,  etc.  (VHI) 


[  Boatmen  and  canalmen(ym) 
|  Janitors  and  sextonB  (V) 
I  Hucksters  and  peddlers  (yn) 
I  Bakers  and  coofectionerB(IV) 
:on  and  steel  workers  (IV) 
jpenters  and  joiners(IV) 


(Leather  worUerB(IV) 
|  Tailors(IV) 


|  Blacksraiths(Iy) 

I  Hotel  and  boarding-house  keeper; 


(m) 


I  Mill  and  factory  operative8(textiles)(IV) 


|  Machinists  (IV) 

;  Architects,  arti&ts,  teachers  of  art(Vl) 
1 


nrdencrs,  florists,  nurserymen  and 

^M  Physicians  and  surge"ns(VI) 

I  ' 

11  Merchants  and  dealers  (VII) 

Engineers  and  surveyors  {y I) 
Teachers  in  BchoolB(VI) 
Lawyers  (VI) 

?olicemcn,  watchmen,  and  detective 
Joot  and  shoe  makers  (IV) 
Soldiers,  sailors,  and  marines(U.S.)  (\ 
Collectors,  auctioneers,  and  agents(II) 
Steam  railroad  employecs(VIlI) 
Clergymen  (VI) 
^liners  and  qiiarrymcn(VIIl) 
Farmers,  planters,  farm  laborers (VIII) 
Bankers,  brokers,  officials  of  companies (II) 
lie  'w 


Death  rates  from  consumption,   of  men  in  fifty-three  occupations,  in  the  registration 
states  of  the  United  States,  1900.     (Brandt.) 


PNEUMONOCONIOSIS  281 

It  is  to  be  noted  that  marble  and  stone  cutters  head  the  list. 
The  high  rate  of  tuberculosis  among  them  has  usually  been  ascribed 
to  the  irritation  of  the  respiratory  tract  by  fine  particles  of  stone 
dust.  A  striking  exception  to  the  danger  of  dust  in  occupation  is 
the  relative  freedom  of  miners  and  quarrymen  who  hold  a  position 
so  near  the  bottom  of  the  list. 

The  frequency  of  tuberculosis  among  miners  varies  widely  accord- 
ing to  the  material  mined  and  the  locality,  but  among  coal  miners 
it  is  generally  recognized  that  the  mortality  from  this  disease  is  low. 
Thus  Arnold,1  Parry,2  Tatham,3  Seltman,4  Goldman,5  Dirksen6  and 
others  agree  in  regarding  tuberculosis  as  relatively  uncommon  among 
coal  miners.  Coal  dust  has  even  been  regarded  as  preventing  the 
development  of  phthisis,  and  it  has  been  proposed  to  treat  the 
disease  with  the  inhalation  of  coal  dust.  Wainwright  and  Nichols7 
in  an  investigation  of  the  causes  of  death  among  857  anthracite  mine 
workers,  at  Scranton,  Pennsylvania,  found  that  23.45  per  cent,  died 
of  pulmonary  disease,  and  of  this  number  only  3.37  per  cent,  of 
pulmonary  tuberculosis,  while  in  2656  deaths  among  other  occupied 
males  at  Scranton,  27.86  per  cent,  were  due  to  pulmonary  disease, 
and  of  these  9.97  per  cent,  to  pulmonary  tuberculosis.  Tuberculosis 
is  thus  about  two-thirds  less  frequent  among  these  miners  than  among 
all  other  occupied  males. 

A  greater  incidence  of  pulmonary  disease  can  be  shown  in  towns 
than  in  country  districts,  and  Asher8  contends  that  as  Germany  has 
become  more  industrial,  the  death  rate,  especially  in  acute  pulmonary 
disease,  has  risen,  and  in  explanation  the  increasing  amount  of  smoke 
may  be  held  responsible.  The  larger  the  town,  the  higher  the 
mortality  curves  for  tuberculous  and  non-tuberculous  disease  of  the 
lung. 

These  and  many  other  inquiries  have  shown  that  the  incidence  of 
and  the  mortality  from  pulmonary  disease  is  usually  greater  among 
workers  in  dusty  occupations  than  in  those  engaged  in  occupations 
without  dust  and  in  the  population  at  large.  The  infrequency  of 
pulmonary  disease  among  coal  miners  is  a  striking  and  significant 
exception  which  has  been  vaguely  and  unsatisfactorily  ascribed  to  a 
protective  influence  from  coal  dust  and  soot.  While  it  must  be  granted 
that  under  certain  conditions,  dust  is  a  factor  in  causing  pulmonary 
disease,  yet  it  must  be  regarded  as  only  one  of  many  factors  in  this 
relation.     Among  workers  in  dusty  occupations,  not  only  dusty  air, 

1  Untersuchungen  iiber  Staubinhalation  und  Staubmetastase,  Leipzig,  1885. 

2  Risks  and  Dangers  of  Various  Occupations,  London,  1900. 

3  Oliver's  Dangerous  Trades,  London,  1900. 

4  Burger,  Der  Beziehung  der  Tuberkulose  zu  der  Anthrakose,  Marburg,  1903. 
6  Die  Hygiene  der  Bergmanns,  Halle,  1903. 

6  Arch.  f.  Hyg.,  1903,  No.  11. 

7  The  Relation  Between  Anthracosis  and  Pulmonary  Tuberculosis,  Amer.  Jour.  Med. 
Sci.,  1905,  p.  130. 

8  Der  Einfluss  des  Rauches  auf  die  Atmungsorgane,  Stuttgart,  Enke,  1905. 


282 


DISEASES  OF   THE   LUNGS 


but  close  confinement  in  overcrowded  and  badly  ventilated  rooms, 
long  and  irregular  hours,  overheating,  sudden  exposure  to  extremes 
of  heat  and  cold,  dampness,  excessive  physical  exertion,  constrained 
positions  at  work,  a  low  rate  of  wages,  insufficient  clothing,  poor 
nutrition,  and  not  infrequently  chronic  alcoholism,  must  also  be 
considered.  Of  far  greater  importance  is  the  influence  of  bacteria 
which  deserves  separate  consideration. 

Dust  and  Bacteria. — Not  all  exposed  to  the  inhalation  of  dust  present 
symptoms  during  life  or  show  pathologic  changes  in  the  lungs  after 
death  as  a  result  of  the  infiltration  of  the  tissue  with  foreign  particles. 
The  occurrence  of  pulmonary  pigmentation  from  coal  dust  and  soot 
with  such  frequency  as  to  constitute  a  normal  appearance  of  the 
lung  is  against  the  view  that  particles  of  dust  are  alone  capable  of 

Fig.  39 


Pneumonoconiosis.     Foreign  pigment  in  lung  tissue   with  slight  if   any  reactive 

inflammation  about  it. 


giving  rise  to  serious  disturbances.  Even  when  the  exposure  has  been 
long  and  severe,  as  in  Traube's  first  case  of  charcoal  inhalation, 
there  may  be  no  indication  of  reactive  inflammation  by  the  forma- 
tion of  connective  tissue.  In  Zenker's  report  it  is  noted  that  long 
exposure  to  the  inhalation  of  English  red  gave  rise  to  respiratory 
symptoms  in  only  one  of  the  workers.  The  tolerance  for  dust  by  a 
great  majority  of  the  workers  in  dusty  occupations  is  a  matter  of 
common  experience.  In  one  instance  at  the  Massachusetts  General 
Hospital  (Autopsy  2953)  a  man,  aged  sixty-one  years,  who  in  youth  had 
worked  as  a  stonemason  and  later  as  a  crossing-tender  on  the  railroad, 
gave  no  history  of  cough,  and  examination  of  the  lungs  was  negative. 
He  died  in  consequence  of  cancer  of  the  intestines,  and  microscopic 
examination  of  the  lungs  (Figs.  39  and  40)  showed  marked  infiltra- 


PNEUM0N0CON1OSIS  283 

tlon  of  the  interalveolar  and  perivascular  tissue  with  pigment,  hut  no 
inflammatory  changes.  Invasion  of  the  lung  by  dust  alone  therefore, 
does  not  necessarily  give  rise  to  pulmonary  disease.  There  must 
then  be  some  other  factor.  The  reports  of  pathologic  changes  due  to 
dust  were  for  the  most  part  made  before  the  importance  of  bacteria 
was  appreciated,  and  antedate  the  discovery  of  the  tubercle  bacillus. 
Pulmonary  lesions  when  present  are  those  consistent  with  the  results 
of  bacterial  invasion,  and  the  almost  constant  and  parallel  increase 
in  the  incidence  of  pulmonary  disease  and  of  tuberculosis  among 
workers  in  dusty  occupations  suggests  that  the  combination  of  dust 
and  bacteria  is  an  important  factor.  The  various  conditions  which 
can  be  regarded  as  having  an  influence  on  pulmonary  disease  among 
workers  in  dusty  occupations  are  so  complex  that  it  is  impossible 

Fig.  40 


Pneumonoconiosis.     Foreign  pigment  in   lung  tissue  with  slight  if  any  reactive 
inflammation  about  it. 

accurately  to  estimate  the  importance  of  any  single  factor,  and  yet 
it  seems  more  reasonable  to  ascribe  a  greater  importance  to  bacteria 
than  to  a  difference  in  the  irritating  qualities  of  marble  and  stone 
dust  and  coal  dust  in  the  incidence  of  pulmonary  disease  among 
marble  and  stone  workers  and  coal  miners.  Marble  and  stone- 
cutters are,  for  example,  frequently  at  work  within  doors,  and  dur- 
ing the  colder  months  of  the  year  in  small,  crowded,  unheated,  and 
dusty  spaces.  The  workers  are  likely  to  be  occupied  in  the  midst 
of  dust  and  expectorated  material,  representing  an  accumulation 
extending  over  a  considerable  period.  Such  conditions  are  favorable 
for  the  spread  of  infection  from  one  worker  to  another.  Coal  miners, 
on  the  other  hand,  work  underground  where  the  dampness  and  the 
constant  invasion  of  new  territory  lessen  the  danger  of  the  spread  of 
infected  material. 


284  DISEASES  OF  THE  LUNGS 

Kinds  of  Dust. — Workers  in  dusty  occupations  inhale  material 
which  varies  according  to  the  character  of  the  trade.  Mixed  dust  is, 
however,  common  in  all  occupations. 

Coal  and  Soot. — Dwellers  in  cities,  where  numerous  factories  fill 
the  air  with  smoke,  are  exposed  to  a  much  greater  degree  than  those 
who  live  in  the  country.  Choremen,  chimney-sweepers,  coal-heavers, 
coal-trimmers,  charcoal-burners,  and  coal-miners  are  especially 
subject  to  the  inhalation  of  coal  or  soot.  Lung  disease  resulting 
from  the  inhalation  of  coal  dust  is  known  as  anthracosis,  melanosis, 
phthisis  melanotics,  coal  miner's  lung,  "black  spit,"  etc.  As  already 
stated,  coal-miners  are  not,  however,  more  affected  with  pulmonary 
disease  than  the  community  at  large  and  in  many  statistics  even 
less  so. 

Metallic  Dust. — Occupations  involving  the  finishing  of  metal 
implements  are  dusty,  and  the  grinders  of  cutlery  and  other  steel 
products  may  suffer  from  pulmonary  disturbances  which  have  been 
termed  "steel-grinder's  phthisis,"  "grinder's  asthma,"  and  "grinder's 
rot."  The  dust  is  composed  of  particles  of  steel  and  stone  and  is  most 
abundant  in  the  process  of  "dry"  grinding.  In  the  hafting  of  knives 
by  means  of  an  emery  wheel,  the  dust  is  made  up  of  particles  of  bone, 
steel,  and  stone.  In  file  cutting  by  hand,  owing  to  the  practice  of 
strapping  the  file  to  a  bed  of  lead,  the  dust  of  the  work  shops  contains 
lead,  which  adds  the  danger  of  poisoning  to  that  from  the  inhalation 
of  dust.  To  the  invasion  of  the  lung  by  iron  dust  Zenker  gave  the 
name  siderosis,  wrhich  in  his  case  was  due  to  the  inhalation  of  English 
red.  The  manufacture,  riling,  turning  and  polishing  of  copper,  and 
the  extraction  of  zinc  from  the  ore  are  dusty  occupations.  In  the 
mining  of  such  metals  as  tin  and  gold,  much  dust  may  be  generated 
in  the  process  of  drilling,  blasting,  shovelling,  and  breaking  the  stone, 
especially  when  this  is  done  by  hand.  Oliver1  called  attention  to 
the  high  death  rate  from  phthisis  among  gold-miners  working  on  the 
Rand. 

Stone  Dust. — The  dust  of  railways  and  streets  set  in  motion  by 
automobiles  and  street  cars  is  a  possible  source  of  danger.  In  sub- 
ways there  is  the  mixture  of  street  and  subway  dust,  and  in  the  latter, 
fine  particles  of  iron  ground  from  the  brake-shoes  of  the  cars  and  the 
rails.  The  blasting,  breaking  and  crushing  of  stone,  the  manufacture 
of  millstones  and  the  making  of  china  and  earthenware  are  dusty 
occupations,  and  may  give  rise  to  such  pulmonary  conditions  as  the 
so-called  "stone-mason's  phthisis,"  "ganister  disease,"  and  "potter's 
phthisis."  Lung  disease  due  to  the  inhalation  of  stone  dust  is  known 
as  chalicosis  or  lithosis. 

Organic  Dust. — Such  textile  manufacture  as  the  making  of  goods 
from  cotton,  hemp,  flax,  wool,  silk,  hair,  and  jute,  rope-,  carpet-,  and 
felt-making,  fur-brushing,  rag-sorting  and  rag-cleaning,  flour-milling 

1  Lancet,  June  14,  1902. 


PNEUMONOCONIOSIS  285 

and  cigar  and  snuff  manufacture,  may  be  dusty  occupations.  Pul- 
monary disease  in  consequence  of  the  inhalation  of  cotton  fiber  has 
been  called  byssinosis,  that  following  tobacco  inhalation  tobaccosis. 

Pathology. — Aside  from  the  invasion  of  the  tissue  by  the  kind 
of  dust  to  which  the  individual  has  been  exposed,  there  are  no  special 
pathologic  features.  The  foreign  particles  may  excite  no  changes 
whatever  and  merely  lie  within  the  tissue  as  an  inert  and  indifferent 
substance.  Considerable  variation  in  the  appearance  of  the  lung  is 
presented  in  those  who  have  apparently  been  similarly  exposed.  An 
unusual  degree  of  invasion  in  certain  individuals  may  be  ascribed  to 
weakening  of  the  protective  force  of  the  ciliated  epithelium,  owing 
to  bronchial  catarrh  and  the  blocking  of  the  pulmonary  lymph 
spaces  by  previous  inflammatory  processes,  thus  preventing  the 
migration  of  dust  from  the  lung  to  the  lymph  glands.  The  influence 
of  chronic  inflammation  in  the  arrest  of  pigment  can  be  seen  in  the 
accumulation  of  pigment  masses  about  areas  of  induration,  giving 
them  a  slaty  color. 

In  extreme  cases  of  anthracosis,  a  black  fluid  can  be  expressed 
from  the  bronchi  or  the  section  surface,  parts  or  the  whole  of  the 
lung  may  show  on  section  a  black  mottled  appearance,  and  under- 
lying the  visceral  pleura  may  be  seen  a  network  of  black  pigment  which 
outlines  the  lobular  septa.  Pigment  is  also  seen  at  times  in  the  costal 
pleura  in  the  form  of  lines  running  parallel  with  the  lower  border  of 
the  ribs.  Pigmentation  of  the  costal  pleura  is  probably  due  to  the 
absorption  of  particles  which  have  escaped  from  the  visceral  pleura 
into  the  pleural  cavity.  According  to  Merkel1  in  cases  of  siderosis 
the  color  is  either  black  (magnetic  oxide  of  iron  and  phosphate  of 
iron)  or  red  (oxide  of  iron),  depending  on  the  character  of  the  inhaled 
dust.  In  chalicosis,  byssinosis,  and  tobaccosis  the  lungs  present  no 
special  features.  In  rare  instances,  in  the  lung  of  coal  workers  and 
more  commonly  in  those  exposed  to  the  inhalation  of  iron  and  stone 
dust,  numerous  very  hard  nodules,  varying  in  size  from  that  of  a 
hemp  seed  to  a  pea,  have  been  described.  These  nodules  grate  on 
section  with  the  knife,  have  a  gray-yellowish  color,  and  show  puncti- 
form  and  linear  markings.  In  many  of  them  a  lumen  the  size  of  a 
pin  point  may  be  seen.  These  nodules,  as  Rindfleisch2  maintained, 
are  probably  areas  of  localized  tuberculosis. 

Other  changes  in  the  lungs  correspond  to  the  features  already  de- 
scribed under  subacute  and  chronic  indurative  pneumonia.  Bronchial 
catarrh  is  usually  present.  Bronchiectasis  and  abscess  cavities  are 
not  infrequent.  Emphysema  and  adhesive  pleurisy  are  common. 
The  bronchial  glands  are  often  black  and  indurated. 

Dust  Metastases. — Dust 'is  found  not  only  in  the  lungs,  tracheo- 
bronchial and  cervical  glands  of  those  exposed  to  the  inhalation  of 
dust,  but  at  times,  especially  in  older  persons,  in  the  mesenteric 

1  Handbuch  der  spec.  Path.  u.  Ther.,  Ziemssen,  Bd.  i,  p.  513. 

2  Lehrbuch  d.  path.  Gewebelehre,  Leipzig,  1873,  3  Auflage. 


286  DISEASES  OF  THE  LUNGS 

glands  and  also  in  the  spleen,  liver,  and  kidney.  Soyka1  was  the 
first  to  establish  this,  finding  anthracotic  pigment  in  the  spleen, 
liver  and  kidneys  of  a  patient,  aged  seventy  years,  with  emphysema. 
lie  believed  that  the  pigment  passed  by  way  of  the  tracheobronchial 

glands  to  the  thoracic  dnct  and  thence  into  the  hlood-streani. 
Weigert2  suggested  an  entrance  to  the  circulation  by  rupture  into 
the  blood-stream  of  anthracotic  glands  adherent  to  bloodvessels  at 
i  he  hilns  of  the  lung.  Arnold'5  suggested  such  a  degree  of  atrophy 
in  the  wall  of  the  branches  of  the  pulmonary  artery  that  particles  of 
dust  at  first  lying  in  the  adventitia  might  later  reach  the  subendothelial 
layer  of  the  intima  and  thus  gain  entrance  to  the  circulation.  YYein- 
traud1  ascribed  the  invasion  of  the  abdominal  organs  to  retrograde 
transport  of  particles  through  the  lymph  stream.  Attempts  to  solve 
the  problem  by  animal  experimentation  have  thus  far  proved  unsuc- 
cessful. The  evidence  at  hand  seems  insufficient  to  decide  on  the  way 
in  which  these  metastases  occur,  but  transportation  by  way  of  the 
blood-stream  is  the  most  probable  explanation.  For  a  discussion  of 
the  question,  reference  may  be  made  to  Roth,5  Gartner,6  Askanazy,7 
Ohkubo,8  Beitzke,9  and  Lubarsch.10  No  harmful  affects  are  known 
to  follow  the  deposit  of  pigment  in  the  internal  organs,  but  the  matter 
is  of  some  importance  from  its  bearing  on  the  manner  in  which  bacteria 
enter  the  body. 

Results  of  Changes  in  the  Tracheobronchial  Glands. — Induration, 
necrosis,  cavity  formation,  and  periadenitis  may  be  seen  in  connection 
with  invasion  of  the  glands  by  dust.  Adhesion  of  the  glands  to 
neighboring  structures  may  have  serious  consequences.  Traction 
diverticulum  of  the  esophagus  may  thus  arise.  In  Leichtensterir*sn 
case  there  was  stenosis  of  the  esophagus.  Rupture  into  the  trachea 
or  bronchi  may  cause  aspiration  pneumonia  or  gangrene.  Perfora- 
tion of  the  pericardium  may  give  rise  to  pericarditis.  A  communica- 
tion may  be  established  between  the  esophagus  or  the  great  blood- 
vessels and  the  air  passages,  with  fatal  hemoptysis  as  a  result.  Com- 
pression of  the  trachea  or  bronchi  may  be  followed  by  bronchiectasis  in 
the  territory  supplied  by  the  partially  occluded  passages.    Tiedemann12 

1  Ueber  die  Wanderung  korpuskularer  Elemente  im  Organismus,  Prager  mcd.  Woch., 
1878,  No.  25. 

2  Ueber  den  Eintritt  des  Kohlenpigments  aus  den  Atmungsorganen  in  den  Kreislauf, 
Fort.  d.  Med.,  1883,  No.  14. 

3  Staubinhalation  und  Staubmetastasc,  Leipzig,  1885. 

4  Untersuchung  iiber  Kohlenstaubmetastase,  I.  D.  Strassburg,  1889. 

5  Ueber  Metastasen  von  Kalk,  Fett  and  Kohlenstaub,  Korrespondenzblatt  f. 
Schweizer  Aerzte,  1884,  vol.  xiv. 

c  Ueber  die  Bcziehung  der  schwarzter  Pigment  in  der  Leber,  Milz  und  Niere  f.  d. 
Kohlenstaubablagerung,  I.  D.  Strassburg,  1885. 

7  Zur  Staubverschleppung  und  Staubreinigung  in  den  Geweben,  Zeit.  f.  allg.  Path. 
u.  path.  Anat.,  1900,  Bd.  xvii. 

8  Ueber  die  Intravasation  der  anthracotischen  Pigmentes  in  die  Blutgefassen  der 
Liiii^e,  Virchow's  Arch.,  1908. 

»  Verhandl.  d.  deutsch.  path.  Gesellsch.,  Jena,  1908,  xii,  237.  10  Ibid.,  p.  241. 

«  Dent,  rn.il.  Woch.,  1891,  No.  15,  p.  534. 

12  Ueber  d.  Ursachen  u.  Wirk.  chron.  entziindlichen  Proz.  im  Mediast.,  Deut.  Arch, 
f.  klin.  Med.,  Bd.  xvi,  p.  575. 


PNEUMONOCONIOSIS  287 

reported  narrowing  of  the  superior  vena  cava  and  obliteration  of 
the  azygos  vein.  Immermann1  noted  a  late  systolic  murmur  con- 
tinued into  early  diastole,  of  variable  distribution  and  intensity, 
but  most  constant  over  the  base  of  the  heart,  and  at  times  heard 
also  between  the  scapulae.  Autopsy  showed  a  stricture  of  both 
primary  branches  of  the  pulmonary  artery  in  consequence  of  inter- 
stitial pneumonia.  In  FrankePs2  case  there  was  a  systolic  murmur 
continued  into  diastole,  of  maximum  intensity  in  the  third  right 
intercostal  space  beside  the  sternum,  and  heard  also  inside  the  spine 
of  the  right  scapula.  Autopsy  showed  folding  of  the  principal  branch 
of  the  right  pulmonary  artery  in  consequence  of  an  adhesion  of  an 
indurated  gland  with  it  and  the  bronchus.  In  Sewall's3  case  a  systolic 
murmur  in  the  back,  inside  the  right  scapula,  was  due  to  pressure  on 
the  right  branch  of  the  pulmonary  artery.  Adhesion  of  indurated 
glands  to  the  vagus  or  its  branches  may  give  rise  to  tachycardia  and 
recurrent  laryngeal  paralysis. 

Symptoms. — In  many  cases  there  are  no  symptoms  whatever  which 
can  be  ascribed  to  the  inhalation  of  dust.  Patients  may  inhale  dust 
for  long  periods  without  pulmonary  symptoms,  and  even  persons 
who  show  large  amounts  of  dust  in  the  lungs  and  bronchial  glands 
after  death,  may  have  had  no  pulmonary  disturbance  during  life. 
Symptoms  when  present  are  similar  to  those  observed  in  cases  with 
bronchitis,  bronchiectasis,  emphysema,  subacute,  and  chronic  indura- 
tive pneumonia  and  pulmonary  tuberculosis.  The  presence  in  the 
expectoration  of  particles  of  foreign  material  only  deserves  special 
consideration.  Workers  in  coal  dust  expectorate  black  sputum  in 
which  minute  particles  of  a  coal-black  color  can  be  seen.  Gritty 
particles  may  prevent  close  application  of  slide  and  cover -glass.  On 
microscopic  examination  hard  coal  appears  as  fine  granules  of  an 
irregular  shape,  polygonal  plates,  or  less  commonly  spear-,  lancet- 
or  needle-shaped  splinters  varying  in  length  and  thickness.  The 
particles  are  free  or  enclosed  in  epithelial  cells  or  leukocytes.  In 
Traube's  case  the  microscopic  appearance  of  the  particles  indicated 
their  origin  from  charcoal.  In  siderosis  the  color  of  the  sputum  varies 
according  to  that  of  the  inhaled  dust,  being  black  as  in  anthracosis 
when  magnetic  oxide  or  phosphate  of  iron  has  been  inhaled  and  red 
if  the  individual  has  inhaled  the  oxide  of  iron.  The  inhalation  of 
stone  dust  or  organic  dust  usually  has  no  influence  on  the  color  of 
the  sputum.  At  times,  patients  who  have  been  exposed  to  stone 
dust  expectorate  stone-like  concretions. 

Inhaled  particles  of  foreign  material  usually  persist  in  the  sputum 
only  until  those  particles  clinging  to  the  walls  of  the  air  passages  or 

1  Striktur  beider  Hauptaste  der  Lungenart.  u.  ihrer  erst.  Verzweig.  infolge  chron. 
interstit.  Pneum.,  Deut.  Arch.  f.  klin.  Med.,  Bd.  v,  p.  235. 

2  Spec-Path.  u.  Ther.  d.  Lungenkrankheiten,  1904,  p.  512. 

3  An  Extraordinary  Case  of  Anthracosis,  Trans.  Amer.  Climatological  Assoc,  1905, 
vol.  xxi. 


2S8  DISEASES  OF  THE  LUNGS 

ingested  by  phagocytic  cells  are  expectorated.  Particles  which  have 
become  imbedded  in  the  tissue  are  expectorated  only  when  there  is 
ulceration  of  the  parenchyma  of  the  lung.  Elastic  tissue  is  also  then 
present  in  the  sputum. 

In  uncomplicated  cases  of  pneumonoconiosis,  examination  of  the 
lungs  is  negative. 

Diagnosis. — Varying  amounts  of  dust  are  found  in  the  lungs  of  all 
persons  exposed  to  dusty  atmosphere,  its  amount  varying  with  the 
degree  and  duration  of  the  exposure.  Unless  complicated  by  inflam- 
matory changes,  the  absence  of  distinctive  clinical  features  may 
prevent  a  clinical  diagnosis,  but  its  presence  may  be  suspected  from 
the  history  of  exposure.  If  masses  of  disintegrated  lung  tissue  are 
expectorated  the  foreign  particles  may  be  detected.  As  it  is  doubtful 
if  dust  alone  and  without  the  presence  of  bacteria  is  capable  of  giving 
rise  to  serious  pulmonary  lesions,  the  establishment  of  the  presence 
of  dust  in  the  pulmonary  tissue  is  of  little  if  any  importance.  It  is 
probable  that  most,  if  not  all,  cases  classed  as  pneumonoconiosis  are 
more  properly  placed  under  subacute  or  chronic  pulmonary  infections. 
The  most  important  question  in  diagnosis  is  whether  the  pulmonary 
disturbance  is  due  to  infection  with  tubercle  bacilli  or  other  organisms. 

Prophylaxis. — In  the  prevention  of  pulmonary  disease  incident  to 
the  inhalation  of  dust,  other  factors  than  dust  itself  must  be  taken 
into  consideration.  Measures  for  the  relief  and  control  of  patients 
with  pulmonary  tuberculosis  must  be  enforced.  Persons  subject  to 
pulmonary  infection  with  other  organisms  than  tubercle  bacilli  are 
also  a  source  of  danger  and  should  be  instructed  as  to  the  proper  care 
of  the  expectoration.  Individuals  suffering  from  tuberculous  or  non- 
tuberculous  infection  should  be  excluded  from  dusty  occupations. 
Sufficient  air  space,  proper  ventilation,  regular,  and  not  unduly 
long  hours  of  employment,  avoidance  of  sudden  exposure  to  extremes 
of  heat  and  cold,  and  excessive  physical  exertion,  an  adequate 
wage,  nourishing  food,  sufficient  and  proper  clothing,  and  abstinence 
from  alcohol  will  do  much  to  diminish  the  incidence  of  pulmonary 
disease.  Until  the  so-called  dusty  occupations  no  longer  deserve 
the  name,  physicians  should  pass  upon  the  fitness  of  candidates, 
and  no  person  under  eighteen  years  should  be  allowed  in  such  employ- 
ment. The  dangers  of  dust  need  especially  to  be  appreciated  by 
workers  in  dusty  occupations,  and  it  is  doubtful  if  the  conditions 
obtaining  in  many  workshops  and  factories  would  long  be  tolerated 
by  the  workers,  or  the  business  continue  to  be  profitable  to  the 
owners  if  the  workers  were  better  informed.  The  distribution  of 
circulars  of  information  among  the  workers  and  owners  would  do 
much  to  correct  unhealthy  conditions.  The  introduction  of  electric 
lighting  in  place  of  gas  and  kerosene,  inlets  of  sufficient  size  for  the 
admission  of  fresh  air,  effective  means  for  the  removal  of  dust,  such 
as  exhaust  fans  with  strong  draught  away  from  the  workers,  daily 


PNEUMONOCONIOfilS  289 

sprinkling  and  sweeping  of  floors,  and  when  necessary,  the  wearing 
of  respirators  will  diminish  the  danger. 

Home  dust,  that  of  public  meeting  places,  and  churches  may  also 
be  dangerous.  Dark,  dirty,  and  ill-ventilated  rooms  may  harbor 
tubercle  bacilli  and  other  organisms  and  prove  a  danger  to  those 
who  inhale  dust  in  such  places.  Dusting  with  a  damp  cloth,  sweeping 
with  a  damp  broom,  and  the  use  of  the  vacuum  cleaner  diminish 
the  chances  of  infection.  The  substitution  for  carpets  of  rugs  which 
may  be  cleaned  outdoors  will  diminish  the  amount  of  house  dust. 
The  use  of  soft  material  in  the  making  of  streets  is  responiible  for 
a  large  amount  of  the  dust  which  gains  entrance  to  city  houses.  In 
streets  where  there  is  much  travel,  especially  by  the  automobile, 
the  amount  of  dust  may  be  enormous.  In  thickly  settled  regions 
asphalt  with  a  hard,  smooth,  and  easily  cleaned  surface  should  be 
substituted  for  macadam.  Sprinkling  with  crude  petroleum  or  the 
use  of  one  of  the  various  preparations  of  tar  on  the  surface  of  soft 
streets  should  be  more  generally  adopted.  The  use  of  soft  coal  for 
heat  and  power  fills  the  air  of  cities  with  smoke,  which  pours  in  black 
clouds  from  the  chimney  tops.  The  use  of  suitable  smoke-consuming 
devices  should  be  required  by  law. 

Treatment. — There  are  no  means  by  which  the  dust  which  has 
invaded  the  lung  can  be  eliminated.  Persons  already  subject  to 
pulmonary  disease  should  avoid  dusty  places,  and  bronchitis,  bronchi- 
ectasis, indurative  pneumonia,  emphysema,  and  other  disturbances 
should  be  appropriately  treated. 


19 


CHAPTER  XVI. 
PULMONARY  ABSCESS  AND  GANGRENE. 

The  clinical  distinction  between  abscess  and  gangrene  is  often 
difficult  or  impossible.  It  may  be  uncertain  even  at  autopsy. 
Typical  examples  of  the  two  affections  may  be  easily  differentiated, 
but  pulmonary  abscess  may  later  develop  into  gangrene,  the  two 
processes  may  be  combined,  and  it  may  be  hard  to  say  where  the 
one  stops  and  the  other  begins. 

Etiology. — In  general  the  same  etiologic  factors  obtain  in  both 
groups.  Although  in  a  considerable  proportion  of  the  cases  the  onset 
is  insidious,  and  the  clinical  findings  fail  to  disclose  the  character 
of  the  underlying  pulmonary  disturbance,  it  is  improbable  that  either 
abscess  or  gangrene  is  ever  actually  primary  and  unpreceded  by 
pulmonary  changes.  In  many  cases,  pulmonary  abscess  and  gangrene 
may  be  recognized  as  secondary  to  infection  of  the  lung,  the  neighbor- 
ing regions  or  more  remote  parts  of  the  body. 

1.  Pulmonary  Infections. — Lobar  Pneumonia.- — Abscess  is  a  clinical 
complication  only  in  rare  instances.  Frankel1  observed  a  termina- 
tion in  abscess  in  scarcely  2  per  cent,  of  1200  cases.  Special  search 
for  pulmonary  abscesses  at  autopsy  on  cases  of  lobar  pneumonia 
shows  that  they  are  not  infrequent  in  fatal  cases.  In  51  cases  of 
lobar  pneumonia  coming  to  postmortem  examination  at  the  Massa- 
chusetts General  Hospital,  abscesses  of  variable  size  were  found 
either  macroscopically  or  microscopically  in  14,  and  doubtless  capable 
of  spontaneous  resolution  in  a  considerable  proportion  of  the  cases. 
The  conditions  in  fatal  cases  are  probably  more  favorable  for  their 
development.  Debility,  alcoholism,  and  general  or  local  circulatory 
disturbances  may  be  in  part  responsible.  Traube2  suggested  emphy- 
sematous degeneration,  to  which  pressure  of  the  pneumonic  exudate 
is  superadded,  as  a  predominant  factor  in  diminishing  the  blood- 
supply  to  an  extent  incompatible  with  survival  of  tissue.  Less 
commonly  he  believed  that  hemorrhage  into  the  inflamed  region 
may  precede  and  in  conjunction  with  the  exudate  cause  sufficient 
compression  to  induce  the  necrosis.  Hemorrhagic  infarction  follow- 
ing local  thrombosis  may  thus  be  a  cause.  Lobar  pneumonia  is  the 
most  easily  recognized  and  appears  to  be  the  most  frequent  single 
cause  of  pulmonary  abscess.  Of  50  cases  of  pulmonary  abscess  at 
the  Massachusetts  General  Hospital,   14  could  be  traced  to  this. 

1  Dcut.  med.  Woch.,  Vereins  Beilage.,  1903,  p.  204. 

2  Gcsammelte  Beitrage  z.  Path.  u.  Physiol.,  1871,  Bd.  ii,  p.  537. 


PULMONARY  ABSCESS  AND  GANGRENE  291 

In  Tuffier's'  series  of  id  operated  cases  of  pulmonary  abscess,  lobar 
pneumonia  was  a  cause  in  23.  Gangrene  appears  to  be  less  frequent 
than  abscess  after  pneumonia.  Aufrecht2  did  not  observe  a  termination 
in  gangrene  in  1501  cases  of  croupous  pneumonia.  Among  Frankel's3 
85  cases  of  gangrene  only  3  could  be  traced  to  genuine  fibrinous 
pneumonia.  Of  50  cases  of  gangrene  at  the  Massachusetts  General 
Hospital,  8  were  apparently  due  to  this  cause. 

Bronchopneumonia. — Owing  to  the  difficulty  of  detecting  small 
areas  of  bronchopneumonia  its  importance  is  hard  to  estimate  in 
clinical  cases.  In  a  series  of  85  cases  of  bronchopneumonia  coming 
to  autopsy  at  the  Massachusetts  General  Hospital,  pulmonary 
abscesses  of  varying  size  were  found  in  16  (macroscopic  in  10,  micro- 
scopic in  6).4  The  cases  represented  for  the  most  part  infection  with 
two  or  more  organisms,  among  which  pneumococci,  the  pyogenic 
cocci  and  influenza  bacilli  predominated.  The  prevalent  belief  that 
abscesses  are  more  frequent  after  infection  with  influenza  bacilli  is 
not  borne  out  by  these  cases.  Of  13  postmortem  cases  of  broncho- 
pneumonia, with  influenza  bacilli  and  other  organisms,  small  abscesses 
were  present  in  only  2.  Many  of  the  cases  of  pulmonary  abscess 
with  an  insidious  onset  should  be  classed  in  this  group.  Those  which 
follow  bronchitis,  bronchiectasis,  etherization,  and  the  inhalation 
of  foreign  bodies  are  usually  due  to  the  breaking  down  of  areas  of 
latent  or  obvious  bronchopneumonia.  Gangrene  as  well  as  abscess 
may  thus  arise.  Abscess  formation  may  precede  the  development 
of  gangrene.  Putrid  bronchitis  and  bronchiectasis  are  specially 
likely  to  give  rise  to  gangrene.  Among  60  cases  of  gangrene  noted 
by  Lenhartz5  9  cases  (15  per  cent.)  were  due  to  bronchiectasis. 

Aspiration.— The  inhalation  of  infected  material  into  previously 
sound  parts  of  the  lung  undoubtedly  plays  an  important  part  not 
only  in  initiating  pulmonary  abscess  or  gangrene,  but  also  in  the 
development  of  multiple  from  single  foci.  The  character  of  the 
aspirated  material  may  determine  the  formation  of  abscess  or  gangrene 
in  the  infected  region.  The  inhalation  of  foreign  bodies,  of  a  solid, 
semisolid,  or  fluid  consistency,  and  pathologic  products  of  suppura- 
tive lesions  are  very  likely  to  give  rise  to  destructive  pulmonary 
lesions.  Submersion  is  not  infrequently  followed  by  abscess  or 
gangrene.  Food  on  its  way  to  or  from  the  stomach  may  be  drawn 
into  the  lungs.  This  may  occur  in  health.  It  is  more  common  during 
unconsciousness  and  sometimes  happens  in  the  insane.  Of  patho- 
logic products,  those  arising  in  the  course  of  diphtheria  of  the 
pharynx  or  larynx,  cancer  of  the  tongue   or  jaw,  ulceration,  new 

1  Chirurgie  du  Pournon.,  Paris,  1897. 

2  Nothnagel's  Encyclopedia  of  Practical  Medicine,  Diseases  of  the  Bronchi,  Lungs, 
and  Pleura,  1902,  p.  760. 

3  Spec.  Path.  u.  Ther.  d.  Lungenkrankheiten,  1904,  p.  546. 

4  Lord,  Boston  Med.  and  Surg.  Jour.,  May  11  and  18,  1905. 

6  Kissling,  Jahrbiicher  der  Hamburgischen,  Staatskrankenanstalten,  Jahrgang,  1905- 
06,  Bd.  x,  p.  10. 


292  DISEASES  OF  THE  LUNGS 

growths  or  traction-diverticula  of  the  esophagus  and  softened  bron- 
chial lymph  glands  perforating  the  trachea  may  be  mentioned.  The 
accident  may  happen  spontaneously,  during  narcosis  for  operation, 
or  in  the  case  of  the  esophageal  lesions  during  the  passage  of  a 
stomach-tube  or  esophageal  bougie.  It  may  follow  tonsillectomy  or 
adenoid  operation.  Gangrene  is  more  likely  to  follow  the  entrance  of 
putrefying  material  into  the  lungs. 

2.  Origin  by  Extension  from  Neighboring  Organs. — Extension  from 
the  bronchi  is  the  most  common  source.  This  has  already  been 
considered.  Infection  of  the  pleura  usually  arises  by  extension  from 
the  lungs,  but  a  purulent  pleurisy  may  in  turn  cause  pulmonary 
reinfection,  with  the  formation  of  pulmonary  abscesses  or  fistulous 
tracts  connecting  the  pleura  and  bronchi.  In  some  instances  the 
adjacent  lung  is  honeycombed  by  the  suppurative  lesions.  It  is 
often  difficult  to  determine  whether  the  pulmonary  abscesses  are 
primary  or  secondary.  Suppuration  in  the  lesser  peritoneum,  the 
retroperitoneal  space  or  the  liver  may  perforate  the  diaphragm  and 
cause  pulmonary  abscesses,  provided,  as  is  often  the  case,  the 
visceral  and  diaphragmatic  pleura?  have  previously  become  adherent. 
Carious  vertebra?,  suppurating  bronchial  glands  and  perforation 
of  the  esophagus  may  likewise  give  rise  to  pulmonary  abscesses  by 
extension.  In  rare  instances  surprisingly  little  pulmonary  damage 
may  follow  the  formation  of  a  fistulous  tract  between  an  outlying 
collection  of  pus  and  the  bronchi.  Gangrene  is  less  common  than 
abscess  in  this  method  of  origin. 

3.  Embolic  Form. — The  clinical  picture  in  this  group  may  be  that 
of  pyemia.  The  detachment  of  infected  thrombi  from  any  part  of 
the  venous  circuit  may  give  rise  to  pulmonary  abscesses;  in  rare 
instances  to  pulmonary  gangrene.  Pulmonary  infarction  may  co- 
exist. At  times,  infection  from  the  bronchi  may  invade  an  area  of 
pulmonary  infarction  due  to  a  bland  embolus.  Ulcerative  endocarditis, 
septic  puerperal  thrombosis  and  thrombosis  of  the  sigmoid  sinus 
complicating  suppurative  disease  of  the  ear  may  be  mentioned  as 
among  the  most  frequent  causes.  Bacteria  or  even  very  fine  emboli 
may  at  times  traverse  the  capillaries.  Endocarditis  of  the  left  side 
of  the  heart  and  pylephlebitis  may  thus  at  times  cause  pulmonary 
infection.  A  certain  proportion  of  the  pulmonary  destructive  lesions 
of  obscure  origin  which  follow  various  operative  procedures,  especially 
abdominal  operations,  are  probably  due  to  the  detachment  of  infected 
thrombi  from  regional  veins. 

4.  Trauma. — Among  50  cases  of  pulmonary  abscess,  trauma  was  a 
cause  in  2.  In  an  equal  number  of  patients  with  gangrene  it  was  a 
cause  in  only  1.  Pulmonary  infection  is  not  common  even  after  chest 
injuries  of  considerable  violence.  Fracture  of  the  ribs  and  contusion 
pneumonia  may  lead  to  these  conditions.  Infection  may  arise  by 
extension  from  without,  as  in  penetrating  wounds  or  from  the  air 
passages.  Laceration  of  the  lung  substance  may  occur  without 
external  evidence  of  thoracic  injury. 


PULMONARY  ABSCESS  AND  GANGRENE  293 

5.  Special  Causes. — Abscesses  of  tuberculous  origin  are  not  under 
consideration  in  this  section,  but  it  should  be  noted  that  the  tubercle 
bacillus,  the  action  of  which  is  usually  if  not  always  reinforced  by 
other  organisms  in  the  production  of  pulmonary  suppuration,  is  the 
most  common  and  important  cause.  Actinomyces  bovis,  like  the 
tubercle  bacillus,  produces  pulmonary  destructive  lesions  and  usually 
in  association  with  other  bacteria.  More  or  less  closely  related  branch- 
ing, filamentous  organisms  variously  described  as  pseudotubercle 
bacilli,  cladothrix  or  atypical  actinomycetes,  and  described  in  the 
section  on  Streptothricosis,  are  also  capable  of  giving  rise  to  similar 
pulmonary  lesions.  Fungi  of  the  genus  Oidium  or  of  the  genus 
Aspergillus,  amebse,  the  lung  fluke,  and  bacillus  mallei  are  rare  causes. 
Syphilitic  pulmonary  lesions  and  new  growths  of  the  lung  may  in 
rare  instances  become  necrotic  with  the  formation  of  abscesses. 
Echinococcus  disease  of  the  lung  or  neighboring  organs  may  likewise 
be  a  factor.  In  all  destructive  processes  in  the  lung,  such  organisms 
as  the  pneumococcus,  the  pyogenic  cocci,  the  influenza  bacillus,  etc., 
are  more  or  less  constantly  present  as  secondary  invaders  singly  or 
combined.  How  far  they  may  be  concerned  as  principal  factors  in 
inducing  pulmonary  suppuration  is  difficult  to  estimate. 

Gangrene  has  been  ascribed  to  different  organisms,  none  of  which 
can  as  yet  be  regarded  as  having  a  specific  etiologic  relationship 
with  the  disease.  In  the  present  state  of  our  knowledge,  gangrene 
may  be  regarded  either  as  dependent  on  the  one  hand  upon  serious 
interference  with  the  blood-supply,  it  may  be  from  unusually  extensive 
thrombosis  in  connection  with  infection  with  pathogenic  bacteria, 
or,  on  the  other,  as  due  to  infection  with  one  or  more  organisms  singly 
or  in  combination  capable  of  causing  a  special  type  of  destructive  and 
putrefactive  pulmonary  lesion.  Attention  has  been  directed  toward 
spirochsetse  as  a  cause.  Feldmann1  found  spirochsetee  by  Levaditi's 
method  of  staining  at  the  margin  of  the  necrosis.  Buday2  finds  a 
large  number  and  great  variety  of  organisms  in  the  gangrenous  parts, 
and  among  them  cocci,  bacilli,  filamentous  organisms,  comma  bacilli, 
fusiforms,  and  spirochaetse.  In  bronchogenous,  acute  gangrene, 
especially  in  those  of  progressive  character,  fusiforms,  comma  bacilli, 
and  spirochsetse  were  present  in  the  tissue  in  the  great  majority  of 
the  cases  and  in  increased  numbers  at  the  margin  of  the  necrosis. 
Identification  of  the  type  of  spirochseta  is  hardly  possible  on  mor- 
phologic grounds  alone. 

Pathology. — On  inspection,  pulmonary  abscesses  appear  as  circum- 
scribed, grayish,  yellowish,  yellowish-green,  greenish,  or  reddish- 
brown  areas,  from  which  pus,  with  or  without  shreds  of  pulmonary 
tissue,  can  be  expressed.  The  pus  may  be  odorless  or  foul.  Single 
cavities  are  usually  more  or  less  round  and  vary  greatly  in  size  from 
beyond  the  limits  of  unaided  vision  to  losses  of  pulmonary  substance 

1  Wiener  klin.  Woch.,  1906. 

2  Beitr.  z.  path.  Anat.  u.  z.  allg.  Path.,  1910,  xlviii,  70. 


294  DISEASES  OF  THE  LUNGS 

involving  the  greater  part  of  one  lobe.  They  may  be  single  or  multiple. 
The  walls  of  fresh  abscesses  or  those  actively  progressing  are  likely 
to  be  soft,  uneven,  and  necrotic,  with  but  little  if  any  line  of  demarca- 
tion between  the  abscess  proper  and  the  surrounding  tissue.  The  walls 
of  older  and  more  quiescent  abscesses  may  be  grayish-white  or  gray, 
brown  or  even  almost  black  in  color,  smooth  or  uneven  and  trabecu- 
lated,  and  dense  from  the  formation  of  connective  tissue.  The  con- 
nective-tissue envelope  may  be  thin  or  thick,  well-  or  ill-defined. 
Confluence  of  neighboring  areas  may  give  rise  to  irregularly  shaped 
excavations.  In  recent  cases  the  surrounding  lung  tissue  is  always 
inflamed.  In  older  processes,  organization  may  have  taken  place 
with  the  formation  of  grayish,  smooth,  tough,  airless  tissue.  Under 
favorable  conditions,  the  contents  of  the  cavity  may  be  expectorated, 
contraction  of  scar  tissue  leads  to  gradual  diminution  in  size,  and 
in  rare  instances,  the  walls  of  small  excavations  may  thus  be  brought 
together  with  final  obliteration  of  the  cavity.  Fibrinous  or  purulent 
pleurisy  may  complicate  pulmonary  abscesses  at  the  periphery  of  the 
lung.    Pyopneumothorax  may  also  occur. 

The  microscopic  study  of  sections  from  cases  of  lobar  or  broncho- 
pneumonia not  infrequently  shows  in  isolated  regions  the  disappear- 
ance of  the  normal  alveolar  arrangement  and  its  replacement  by 
pus  cells  representing  the  beginnings  of  small  abscesses.  Such  micro- 
scopic areas  of  suppuration  are  probably  capable  of  restoration  to 
functional  integrity.  In  more  advanced  abscess  formation,  the  con- 
tents of  the  cavities  may  be  found  to  consist  of  well-preserved  or 
disintegrated  pus  cells,  detritus,  and  bacteria  of  various  kinds,  with 
elastic  fibers  and  shreds  of  pulmonary  tissue.  The  walls  of  the  abscess 
cavity  and  the  neighboring  pulmonary  tissue  are  infiltrated  with 
pus  cells.  In  the  more  subacute  and  chronic  cases,  the  formation 
of  new  fibrous  tissue  from  the  neighboring  interalveolar  septa,  the 
interlobular,  peribronchial,  and  perivascular  tissue  may  be  noted. 

Laennec  first  accurately  described  pulmonary  gangrene  and  recog- 
nized a  diffuse  and  a  circumscribed  form.  Diffuse  gangrene  is  rare. 
Laennec  saw  but  two  cases  in  twenty-four  years.  The  greater  part 
or  the  whole  of  one  lobe  may  be  involved  and  converted  into  a  greenish- 
black,  pulpous,  foul-smelling  mass,  with  ill-defined  boundaries.  In 
the  more  common  circumscribed  variety,  single  or  multiple  areas  are 
found.  They  vary  in  size  from  a  bean  to  an  apple,  at  first  are  dry 
and  greenish-gray  in  color,  later  moist,  softened,  greenish-brown  or 
black,  extremely  offensive,  and  in  places  disintegrated  with  the  forma- 
tion of  cavities.  The  cavities  contain  a  brownish  or  greenish,  offensive 
fluid,  and  are  lined  with  uneven,  shreddy  walls.  Evacuation  of  the 
contents  may  show  bronchi  and  bloodvessels,  especially  arteries, 
lining  their  walls  or  traversing  the  lumen.  The  bloodvessels  are 
usually  extensively  thrombosed.  If  erosion  of  a  vessel  precedes  its 
occlusion,  severe  and  even  fatal  hemorrhage  may  result.  The  gan- 
grenous area  may  be  sharply  differentiated  from  the  surrounding 


PULMONARY  ABSCESS  AND  GANGRENE  295 

tissue  by  a  zone  of  intense  hyperemia  or  more  firmly  consolidated 
tissue,  beyond  which  there  is  pulmonary  edema  for  a  variable  distance. 
In  slowly  progressive  or  stationary  lesions,  a  pyogenic  membrane 
may  form  outside  the  gangrenous  region.  In  favorable  cases,  the 
necrotic  and  disintegrated  material  may  be  absorbed  or  expectorated, 
organization  and  connective-tissue  formation  take  place,  the  cavity 
slowly  diminishes  in  size  and  may  finally  heal.  In  less  favorable 
instances,  it  remains.  In  chronic  cases,  induration  of  the  neighboring 
tissue  is  an  invariable  accompaniment,  in  spite  of  which,  however, 
the  process  may  continue  slowly  to  extend.  In  long-standing  disease, 
bronchiectasis  occurs  in  the  bronchi  communicating  with  the  diseased 
region.  Fibrinous,  serofibrinous,  purulent  or  putrid  pleuritis,  and 
pyopneumothorax  may  complicate  acute  pulmonary  gangrene  situated 
near  the  periphery  of  the  lung.  Extensive  pleural  adhesions  are  likely 
to  form  in  the  course  of  more  chronic  cases.  Multiple  gangrenous 
foci  are  common  and  arise  by  extension  or  aspiration.  The  bronchial 
mucous  membrane  is  reddened  and  swollen  in  consequence  of  irrita- 
tion from  contact  with  the  decomposing  material.  The  bronchial 
lymph  glands  are  usually  enlarged.  Single  or  multiple  cerebral 
abscesses  may  arise  from  the  detachment  of  infected  thrombi  from 
the  pulmonary  veins. 

Microscopic  examination  of  sections  from  acute  cases  of  pulmonary 
gangrene  shows  serum,  scanty  fibrin,  occasional  leukocytes,  and 
desquamated  epithelial  cells,  and  usually  an  abundance  of  red  blood 
corpuscles  within  the  alveoli.  In  places,  fibrin  and  pus  cells  may  be 
more  abundant.  Connective-tissue  formation  may  be  noted  in  the 
neighboring  lung  as  already  mentioned  in  connection  with  pulmonary 
abscess. 

Certain  pathologic  features  of  abscess  and  gangrene,  such  as  (1)  the 
site  of  the  lesions,  (2)  their  number,  (3)  the  occurrence  of  pulmonary 
induration,  and  (4)  the  condition  of  the  pleura,  deserve  special  mention. 
In  this  connection  the  two  processes  may  well  be  considered  together. 

1.  The  Site  of  the  Lesions. — Abscess  or  gangrene  may  be  found  in 
any  part  of  the  lung.  The  lower  lobes,  and  especially  the  right,  are 
more  frequently  involved.  Proximity  to  the  pleura  is  in  general  a 
striking  feature.  Of  30  cases  coming  to  postmortem  examination 
at  the  Massachusetts  General  Hospital  the  lesions  were  just  beneath 
or  extended  into  the  pleura  in  28.  In  one  of  the  remaining  cases, 
with  multiple  processes,  their  relation  was  variable,  some  near  and 
others  distant  from  the  pleura,  while  in  the  last  case  they  were  deep 
within  the  substance  of  the  lung.  Their  deep  or  superficial  site  varies 
somewhat  with  the  cause.  Foreign  bodies  lodged  in  the  larger  bronchi 
are  likely  to  lead  to  deep-seated  processes.  Following  trauma,  they 
may  be  found  at  the  seat  of  the  injury.  Extension  from  neighboring 
extrapulmonary  regions  affects  the  nearby  parts  of  the  lungs. 

2.  The  Number  of  the  Lesions. — Pulmonary  destructive  processes 
are  more  often  multiple  than  single.    Thus  of  38  cases  of  abscess  or 


296  DISEASES  OF  THE  LUNGS 

gangrene  coming  to  autopsy  a  single  focus  was  found  in  13,  multiple 
foci  in  25.  The  cause  of  the  process  bears  an  uncertain  but  somewhat 
suggestive  relation  to  the  number  of  the  lesions.  Bronchopneumonia, 
aspiration  pneumonia,  and  embolism  are  more  likely  to  lead  to 
multiple  and  widely  separated  lesions.  Croupous  pneumonia  is  like- 
wise more  often  followed  by  multiple  foci,  as  in  2  of  3  cases  in  the 
series,  but  limitation  to  one  lobe  may  be  more  often  observed.  The 
duration  of  the  process  is  of  greater  importance.  This  is  strikingly 
illustrated  in  11  operated  cases  at  the  Massachusetts  General  Hospital. 
Of  6  patients  with  a  history  of  from  three  weeks  to  two  months  the 
findings  at  operation  and  the  rapid  subsidence  of  cough  and  expectora- 
tion thereafter  in  5  indicate  that  the  evacuated  pus  was  probably 
from  the  only  important  focus.  Of  5  other  cases  with  symptoms 
for  from  nine  months  to  four  years,  the  pulmonary  lesions  were  cer- 
tainly or  probably  multiple  in  4.  In  general,  it  may  be  said  that  acute 
abscess  or  gangrene  is  single  or  predominantly  confined  to  one  region. 
But  the  longer  the  process  has  lasted,  the  greater  is  the  opportunity 
for  the  formation  of  multiple  foci,  by  extension  into  contiguous  territory 
or  aspiration  into  neighboring  or  remote  parts  of  the  lungs.  Chronic 
processes  are  thus  almost  invariably  multiple. 

3.  Pulmonary  Induration. — Here,  too,  the  duration  of  the  disease 
is  a  most  important  consideration.  In  the  acute  cases  the  affected 
regions  are  not  sharply  limited  from  the  surrounding  and  always 
inflamed  pulmonary  tissue.  In  the  more  subacute  and  chronic  cases 
the  adjacent  zone  of  reactive  pneumonia  is  gradually  transformed 
into  granulation  tissue,  which  later  gives  place  to  connective  tissue. 
Pulmonary  induration  may  be  diffuse  or  confined  to  the  immediate 
neighborhood  of  the  destructive  process.  Bronchiectasis  and  multiple 
lesions  are  frequently  observed.  It  is  impossible  to  state  the  necessary 
interval  for  the  development  of  induration,  since  it  varies  in  different 
cases.  In  one  of  the  hospital  series,  marked  interstitial  pneumonia 
was  found  about  a  large  abscess  cavity  three  and  one-half  wTeeks 
after  an  apparent  lobar  pneumonia. 

4.  The  Condition  of  the  Pleura. — The  frequent  peripheral  site  of 
pulmonary  abscess  and  gangrene  is  responsible  for  pleural  involve- 
ment in  a  majority  of  cases.  The  proportion  varies  in  different  series. 
Turner's  figures  are  usually  quoted.  He  noted  pleural  adhesions  in 
87  per  cent.  In  35  cases  coming  to  postmortem  examination  at  the 
Massachusetts  General  Hospital  the  visceral  and  parietal  layers 
were  firmly  adherent  in  the  region  of  the  pulmonary  process  or  over 
a  wider  area  in  13,  purulent  pleuritis  was  present  in  5,  weak  adhesions 
or  a  few  bands  of  connective  tissue  were  found  in  12,  and  the  lungs 
were  free  in  the  remaining  5.  The  cause  of  the  pulmonary  lesions 
may  determine  the  condition  of  the  pleura.  Croupous  pneumonia 
and  extension  of  suppuration  from  without  never  spare  the  pleura. 
If  the  disease  is  due  to  bronchopneumonia,  aspiration  pneumonia, 
or  embolism  the  pleura  may  be  free. 


PULMONARY  ABSCESS  AND  GANGRENE  297 

Symptoms. — The  symptoms  of  abscess  differ  from  those  of  gangrene 
principally  in  degree.  Abscess  is  a  much  milder  and  simpler  process. 
The  clinical  features  of  abscess  will  first  be  considered,  but  it  must 
be  constantly  in  mind  that  a  sharp  distinction  between  them  cannot 
be  made.  In  some  instances,  the  two  diseases  may  represent  in  a  single 
case  a  beginning  as  abscess,  which  later  develops  into  gangrene;  in 
others,  the  opposite  relation  may  obtain. 

1.  Abscess. — When  lobar  pneumonia  terminates  in  abscess,  the  first 
intimation  may  be  a  persistence  of  fever  after  the  time  of  its  expected 
decline,  an  accession  of  cough,  a  more  abundant  purulent  sputum, 
and  the  failure  of  resolution  in  the  affected  lung.  The  temperature 
is  usually  irregular,  but  often  shows  marked  morning  remissions  and 
evening  exacerbations.  It  may  be  remittent  or  intermittent  and  is 
sometimes  absent.  The  cough,  aside  from  becoming  more  frequent 
and  harassing,  may  lack  distinctive  features.  The  sputum  changes 
from  rusty,  tenacious,  to  mucopurulent,  and  later  to  purulent;  from 
scanty  to  an  increasingly  more  abundant  expectoration.  There  may 
be  frequently  recurring  chills.  The  patient  is  likely  to  become  pale 
and  lose  in  weight  and  strength.  There  may  be  no  distinctive  physical 
signs,  and  for  some  days  to  a  week  or  more  the  suspicion  of  caseous 
pneumonia,  empyema,  pulmonary  induration  or  abscess  may  be 
entertained.  In  typical  cases,  however,  a  more  severe  paroxysm  of 
cough  may  be  followed  by  the  sudden  expectoration  of  a  large  amount 
of  pus,  after  which  the  physical  signs  of  cavity  may  be  found  and 
the  symptoms  immediately  improve.  The  purulent  sputum  continues, 
but  may  gradually  diminish  in  amount.  Small  cavities  may  com- 
completely  heal. 

The  symptoms  of  abscess  following  bronchopneumonia  or  aspira- 
tion pneumonia  present  little  that  is  characteristic.  To  the  clinical 
features  of  these  conditions  may  be  added  a  more  severe  cough,  fever 
of  a  septic  type,  and  the  sudden  expectoration  of  abundant  sputum. 
The  embolic  form  of  abscess  is  likely  to  be  masked  by  the  severity 
of  the  underlying  general  infection.  When  pulmonary  suppuration 
supervenes  on  hemorrhagic  infarction  the  bloody  sputum  becomes 
mixed  with  or  ch'anges  to  pus.  Evacuation  may  occur  suddenly  as  in 
other  forms.  The  symptoms  of  pulmonary  abscess  arising  by  extension 
from  without  are  often  obscure.  The  pus  may  invade  the  lung  in 
many  small  areas  over  a  considerable  territory,  with  only  a  gradual 
increase  in  already  existing  pulmonary  symptoms.  Obvious  perfora- 
tion may,  however,  occur.  It  may  be  followed  by  evident  relief  and 
insignificant  symptoms.  In  some  instances  serious  symptoms  of  suffo- 
cation and  even  death  may  quickly  follow. 

The  most  suggestive  single  symptom  of  pulmonary  abscess  is  the 
sudden  expectoration  of  a  large  amount  of  pus.  The  patient  is  often 
conscious  of  the  sudden  relief  of  pressure  and  may  even  indicate  its 
site.  With  the  development  of  a  cavity  communicating  with  the 
bronchi,  paroxysmal  cough,  and  the  evacuation  within  a  short  period 


L".is  DISEASES  OF  THE  LUNGS 

of  considerable  amounts  of  sputum  is  often  a  striking-  feature.  It  is 
especially  common  in  the  more  subacute  or  chronic  eases,  and  the 
patient  may  be  almost  or  quite  free  from  cough  in  the  intervals.  Such 
periodic  evacuation  depends  on  imperfect  drainage,  and  is  more  often 
seen  with  abscesses  in  the  lower  lobes  of  the  lungs.  The  assumption 
of  certain  positions,  such  as  lying  on  the  unaffected  side,  may  constantly 
induce  a  paroxysm,  while  maintenance  of  the  cavity  in  a  dependent 
part  of  the  lung  may  insure  the  greatest  relief.  Patients  with  cavities 
in  one  or  the  other  lower  lobes  may  thus  be  most  comfortable  in  a 
sitting  or  half-sitting  position  and  inclined  toward  the  affected  side. 
Similar  paroxysmal  evacuation  may  be  seen  with  bronchiectasis.  The 
breath  may  have  a  disagreeable  odor.  Pain  from  pleurisy  is  frequent. 
Dyspnea  is  not  a  striking  feature  from  abscess  alone. 

Sputum. — This  is  mucopurulent  or  purulent.  It  is  very  variable 
in  amount  and  may  reach  several  hundred  to  five  hundred  cubic 
centimeters  or  more  in  twenty-four  hours.  The  color  is  a  varying 
shade  of  green.  Admixture  of  blood  may  give  a  brownish  tinge. 
Pure  blood  may  be  expectorated  in  streaks  or  as  frank  hemorrhage. 
The  sputum  may  be  odorless  or  disagreeable  and  variously  described 
as  stale,  musty,  sweetish  or  even  fetid,  but  not  horribly  offensive 
as  in  pulmonary  gangrene.  The  odor  alone  is  not  a  safe  means  of 
distinguishing  the  two  processes.  If  the  disease  is  of  short  duration, 
putrid  sputum  suggests  gangrene.  Putrefaction  of  shreds  of  pul- 
monary tissue  lining  the  walls  of  abscesses  or  the  purulent  contents 
of  the  cavity  may  likewise  give  rise  to  a  foul  odor.  In  chronic  abscesses 
and  in  bronchiectasis,  putrid  sputum  is  occasionally  observed  from 
the  latter  cause.  The  gross  appearance  of  the  sputum  may  suggest 
its  source.  Pus  from  large  and  single  abscesses  or  from  outlying  sup- 
puration is  likely  to  be  homogeneous  and  little  mixed  with  mucus. 
Sputum  from  multiple  abscesses,  on  the  contrary,  may  show  little 
tendency  to  confluence,  each  mass  being  covered  with  mucus.  Too 
much  reliance  should  not  be  placed  on  such  features,  however,  for  the 
abscess  may  communicate  imperfectly  or  not  at  all  with  the  air  pas- 
sages and  mucus  covered  masses  of  sputum  may  come  from  inflamed 
bronchi.  An  almost  pure  purulent  sputum  with  little  admixture  of 
mucus  may  occur  in  advanced  bronchiectasis,  with  loss  of  the  bron- 
chial mucous  glands.  A  conclusion  as  to  the  size  of  the  cavity  from 
the  amount  expectorated  at  one  time  is  uncertain,  as  the  cavities  may 
be  multiple  and  a  portion  of  the  sputum  may  also  come  from  other 
parts  of  the  inflamed  lung  or  the  bronchi. 

After  standing  the  sputum  may  separate  into  three  layers :  a  sediment 
of  pus  at  the  bottom,  a  layer  of  foamy  mucus  more  or  less  intermixed 
with  mucopurulent  masses  at  the  top,  and  thin,  cloudy  fluid,  mostly 
saliva,  in  the.  intervening  space.  Similar  stratification  of  the  sputum 
on  standing  may  be  seen  in  bronchiectasis  or  the  evacuation  of  pus 
through  the  bronchi  from  without,  as  from  empyema. 

Careful  examination  of  the  sputum,  if  necessary  in  a  flat  glass  dish 


PULMONARY  ABSCESS  AND  GANGRENE  299 

on  a  black  background,  may  disclose  shreds  or  masses  of  pulmonary 
tissue.  If  the  specimen  has  been  standing  the  sediment  is  most  likely 
to  contain  them.  They  vary  from  microscopic  dimensions  to  masses  an 
inch  or  more  in  length,  at  times  of  a  reddish  color,  but  more  often 
yellowish-white  or  greenish-gray  from  infiltration  with  pus.  Their 
origin  from  the  lung  may  be  determined,  on  microscopic  examination, 
by  the  presence  of  elastic  tissue.  They  may  also  contain  fatty  acid 
crystals,  pigment,  and  abundant  bacteria.  Small  grayish-white  or 
yellowish  particles  or  granules  may  be  found  in  the  sediment  of  pus. 
They  can  be  differentiated  from  actinomyces  granules  only  by  the 
microscope.  When  crushed  between  cover  glass  and  slide,  they  are 
found  to  consist  almost  exclusively  of  bacteria.  They  are  smaller 
than  Dittrich's  plugs. 

Elastic  Tissue. — This  may  be  found  in  the  shreds  of  pulmonary 
tissue.  Smaller  particles  of  elastic  tissue,  visible  only  with  the  micro- 
scope, are  more  common.  Its  presence  is  a  certain  indication  of  a 
destructive  lesion.  It  may  be  demonstrated  by  Sir  Andrew  Clark's 
method  as  recommended  by  Osier.  The  thick  purulent  sputum  is 
poured  upon  a  glass  plate  15  x  15  cm.,  flattened  into  a  thin  layer  by 
means  of  a  second  plate  10  x  10  cm.  and  examined  over  a  black  back- 
ground. Elastic  tissue  appears  as  grayish-yellow  spots  and  may  be 
identified  under  the  low  power  of  the  microscope.  Only  the  larger 
masses  can  be  recognized  in  this  way.  Smaller  fibers  must  be  sought 
under  the  high  power. 

Elastic  tissue  appears  under  the  microscope  as  intensely  refractive 
fibers  or  bundles  of  fibers,  with  a  sharply  defined,  wavy  outline.  The 
fibers  are  of  varying  but  usually  small  diameter  and  frequently  branch. 
Their  ends  are  often  curled  and  frayed.  An  origin  from  the  lung  can 
be  determined  with  certainty  only  when  an  alveolar  arrangement  can 
be  shown.  Destructive  processes  in  the  larynx,  trachea,  bronchi  or 
pleura  may  also  give  rise  to  single  or  interlacing  filaments  of  elastic 
tissue. 

For  the  discovery  and  identification  of  small  fragments  of  elastic 
tissue  I  have  generally  used  the  following  method  of  sedimentation 
and  staining:  From  0.5  c.c.  to  1  c.c.  of  the  thick,  purulent  sputum 
'  is  placed  in  a  small  Erlenmeyer  flask  and  diluted  with  15  to  20  volumes 
of  distilled  water.  A  few  drops  (3  to  5)  of  KOH  are  added  and  the 
mixture  gently  warmed  over  the  Bunsen  flame  until  the  sputum  is 
dissolved.  As  small  an  amount  of  KOH  as  possible  should  be  used 
in  order  to  keep  the  specific  gravity  low.  Elastic  tissue  is  insoluble1 
in  KOH.  The  solution  is  then  sedimented  by  means  of  the  centri- 
fuge, the  supernatant  fluid  decanted  and  smears  made  on  cover- 
glasses  by  means  of  the  platinum  loop  from  the  small  amount  of  sedi- 
ment which  remains.  The  smears  are  dried  in  the  air  or  over  the  Bunsen 
flame,  fixed  by  heat,  as  for  tubercle  bacilli,  and  covered  with  Weigert's 

1  In  acids  and  alkalis. 


300 


DISEASES  OF  THE  LUNGS 


elastic  tissue  stain.1  A  convenient  method  is  to  slip  the  cover-glass 
into  a  large  test-tube  containing  enough  of  the  stain  to  cover  it.  'Flic 
action  of  the  stain  can  be  accelerated  by  heat,  but  a  water  bath  must 
be  used  or  the  alcohol  in  the  preparation  will  ignite.  Immersion  of  the 
end  of  the  test-tube  containing  the  cover-glass  and  stain  in  boiling- 
water  for  about  five  minutes  is  usually  sufficient.  The  preparation  is 
decolorized  in  alcohol  (95  per  cent.),  dehydrated  with  absolute  alcohol, 
cleared  with  xylol  and  mounted  in  Balsam.  The  elastic  fibers  appear 
dark  blue  or  almost  black.  If  cells  are  present  their  shadowy  outline 
may  be  seen. 


Fig.  41 


Fig.  42 


Fig.  43 

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'Nwf           ■       iQ  ^& 

3Efc?* 

#£* 

?' 

Elastic  tissue  in  sputum,  stained  with  Weigert's  elastic  tissue  stain, 
arrangement  is  best  shown  in  Fig.  43. 


An  alveolar 


By  the  use  of  this  method,  confusion  of  elastic  tissue  with  connective- 
tissue,  fatty  acid  crystals,  leptothrix,  chains  of  bacteria,  fragments 
of  cells,  and  vegetable  fibers  may  be  avoided.  Elastic  tissue  from 
food  is  a  possible  source  of  error,  which  may  be  prevented  by  careful 
collection  of  the  sputum. 


1  Centralbl.  f.  allg.  pathologie,   1898,  ix,  289,  or  Mallory  and  Wright's  Pathologic 
Technique. 


PULMONARY  ABSCESS  AND  GANGRENE  301 

2.  Gangrene. — What  has  been  said  of  the  symptoms  of  abscess 
applies  also  to  gangrene.  The  constitutional  depression  may  be  more 
severe,  the  loss  of  flesh  and  strength  more  rapid.  The  gross  and  micro- 
scopic character  of  the  sputum  is  much  the  same.  It  is  much  more 
offensive  than  in  acute  abscess.  Blood,  usually  much  altered,  is  more 
often  present,in  consequence  of  which  the  sputum  is  likely  to  be  reddish, 
dirty  brown,  or  chocolate  in  color.  Severe  and  even  fatal  hemoptysis 
may  occur  both  in  abscess  and  gangrene.  Shreds  of  pulmonary  par- 
enchyma are  more  often  found  in  sputum  from  gangrene  than  from 
abscess.  Traube1  regarded  the  absence  of  elastic  tissue  from  the  shreds 
of  pulmonary  tissue  as  a  characteristic  feature  of  gangrene  and  in 
striking  contrast  to  its  abundance  in  abscess.  Von  Leyden2  in  general 
agreed  with  this  opinion,  but  noted  the  presence  of  elastic  fibers  in 
the  sputum  of  cases  of  gangrene  in  exceptional  instances.  In  my 
experience,  elastic  tissue  is  present  in  about  the  same  proportion  of 
cases  with  gangrene  as  with  abscess.  Dittrich's3  plugs  may  also  be 
found  in  the  sputum.  They  are  soft  and  mushy  or  putty-like  masses, 
varying  in  size  from  a  millet-seed  to  a  bean,  of  an  extremely  offensive 
odor,  and  composed  principally  of  bacteria,  with  fatty  acid  crystals, 
free  fat,  and  debris.  They  are  not  characteristic  of  gangrene,  being 
found  also  in  bronchiectasis  and  occasionally  in  abscess. 

Physical  Signs. — In  a  considerable  proportion  of  cases,  examina- 
tion fails  to  disclose  the  site  of  the  abscess  or  gangrene  even  when  this 
is  circumscribed  and  of  some  extent. 

In  the  acute  cases  of  abscess  or  gangrene  the  persistence  of  rales 
at  one  place  may  suggest  the  site  of  a  developing  process.  A  friction 
rub  may  be  heard.  Slight  variation  from  the  normal  in  the  breathing, 
voice,  and  fremitus  may  be  present.  Dulness  on  percussion  is  common 
to  the  largest  number  of  cases.  It  is  usually  due  to  consolidation  of 
neighboring  lung,  at  times  to  a  complicating  pleurisy  with  exudation. 
In  cases  in  which  there  is  a  collection  of  fluid  in  the  lung  and  before 
a  communication  is  established  with  the  bronchi  in  addition  to  dulness, 
there  is  diminished  breathing,  voice,  whisper  and  tactile  fremitus  over 
the  involved  region.  As  the  destructive  lesion  progresses  and  after 
communication  with  the  bronchi  has  been  established,  changes  in  the 
findings  from  day  to  day  or  after  a  paroxysm  of  cough  may  be  noted. 
A  variation  in  the  auscultatory  signs  is  most  important  and  depends 
on  the  amount  of  pus  retained  in  the  cavity.  If  the  contents  has  been 
evacuated,  the  breathing  may  be  distinctly  bronchial.  Amphoric 
breathing  and  metallic  rales  may  also  be  heard,  but  less  often  in  acute 
than  in  subacute  and  chronic  cases. 

Over  well-developed  and  superficial  cavities  the  signs  may  be  quite 
typical.  The  most  striking  feature  may  be  bronchial  breathing  over 
an  area  tympanitic  on  percussion.     Cracked-pot  note  or  a  variation 

1  Ges.  Beitrage  zur  Path.  u.  Ther.,  1871,  Bd.  ii,  p.  454. 

2  Volkmann's  klinische  Vortrage,  4  Ser.,  pp.  91-120. 

3  Ueber  Lungenbrand  in  Folge  von  Bronchialerweiterung,  Erlangen,  1850. 


302  DISEASES  OF  THE  LUNGS 

in  the  percussion  sound  with  the  mouth  open  and  closed,  during  inspir- 
ation and  expiration  and  on  changing  the  position  of  the  patient  may 
be  noted.  On  auscultation  there  may  be  coarse,  bubbling  or  fine, 
ringing  metallic  rales,  bronchial,  and  amphoric  breathing,  loudly 
increased  bronchial  whisper  and  voice,  with  an  amphoric  quality. 
In  doubtful  cases  it  is  well  to  ask  the  patient  to  cough  and  again 
examine  suspected  areas. 

The  smallest  cavity  detected  as  such  during  life,  in  the  hospital 
series  measured  at  autopsy  3x2  cm.  and  was  situated  just  under  the 
pleura  in  the  posterior  aspect  of  the  left  inferior  lobe.  Larger  cavities 
are  often  missed,  especially  if  deeply  placed  or  without  free  communi- 
cation with  the  bronchi. 

Complications. — Pneumonia  of  the  neighboring  region  is  invariably 
present.  Bronchopneumonia  or  aspiration-pneumonia  are  not  infre- 
quent  and  may  give  rise  to  multiple  areas  of  abscess  or  gangrene. 
Pulmonary  induration  is  induced  by  the  more  subacute  or  chronic 
destructive  processes.  Bronchiectasis  frequently  follows  long-continued 
pulmonary  suppuration. 

Hemoptysis  is  frequent.  The  amount  of  blood  is  usually  small. 
Severe  and  even  fatal  hemorrhage  may  occur  both  in  abscess  and  gan- 
grene. It  occurs  both  in  acute  and  chronic  processes  and  comes  from 
arteries  lining  the  walls  or  traversing  the  lumen  of  cavities.  Fatal 
bleeding  is  more  common  in  gangrene.  Of  50  cases  of  gangrene  at  the 
Massachusetts  General  Hospital  1  was  fatal  from  this  cause.  There 
was  an  enormous  hemorrhage  on  the  twentieth  day  of  the  disease  and 
death  occurred  from  a  recurrence  of  the  bleeding  two  days  later. 
Nordmann1  has  collected  the  instances  of  grave  hemoptysis  found  jn 
the  literature.  An  important  distinction,  I  believe,  may  be  made 
between  the  cases  in  which  hemoptysis  precedes  by  a  longer  or  shorter 
interval  the  development  of  abscess  or  gangrene  and  those  in  which 
it  occurs  during  their  course.  In  the  former  group  the  suspicion  of 
tuberculosis  should  be  strongly  entertained,  provided  other  pulmonary 
symptoms  are  insignificant  or  absent,  while  in  the  latter  a  destructive 
process  of  a  different  etiology  is  a  sufficient  cause. 

Infection  of  the  pleura  may  lead  to  fibrinous,  serofibrinous,  puru- 
lent, or  putrid  pleuritis.  The  milder  forms  are  more  common.  Puru- 
lent or  putrid  exudates  are  more  often  seen  with  gangrene.  An  exuda- 
tive pleuritis  complicated  10  (11.8  per  cent.)  of  Frankel's2  85  cases 
of  gangrene.  A  pneumococcus  empyema  was  present  in  1  and  a  putrid 
exudate  in  the  remaining  9  cases,  3  of  which  were  associated  with 
pneumothorax.  As  Frankel  states,  the  putrid  empyema  may  be  present 
before  the  gangrene  becomes  apparent.  Reactive  inflammation  about 
the  gangrenous  area  and  compression  by  the  pleural  exudate  may 
effectually  close  a  communication  with  the  bronchi.  Disintegration 
of  the  bronchial  wall  may  finally  lead  to  evacuation  of  the  gangrenous 

1  Gaz.  des  Hop.,  1906,  p.  1034. 

2  Spez.  Path.  u.  Ther.  d.  Lungenkrankheiten,  1904,  p.  559. 


PULMONARY  ABSCESS  AND  GANGRENE  303 

cavity  and  the  empyema  through  the  bronchi.  Pericarditis  may  also 
occur.  Clubbing  of  the  fingers  may  complicate  chronic  pulmonary 
abscess  or  gangrene.    (See  Bronchiectasis.) 

Cerebral  abscess  complicates  pulmonary  abscess  or  gangrene  in 
rare  instances.  Virchow1  first  noted  its  association  with  gangrene. 
Sir  William  Gull2  specially  emphasized  the  complication.  Many 
cases  arising  in  the  course  of  suppurative  pulmonary  and  pleural 
disease  have  since  been  reported.  Martius3  in  1891,  collected  22  cases 
with  autopsy,  including  7  reported  by  Naether4  and  2  of  his  own. 
Cameron,5  in  1907,  analyzed  17  cases.  The  cerebral  lesions  are  prob- 
ably due  to  the  detachment  of  infected  emboli  from  thrombi  in  the 
pulmonary  veins.  They  may  be  secondary  to  empyema,  gangrene, 
abscess,  bronchiectasis  or  purulent  bronchitis.  An  interesting  feature 
is  the  apparent  infrequency  of  metastatic  abscesses  in  other  regions 
than  the  brain.  Among  Martius'  22  cases  of  pulmonary  cerebral 
abscess,  metastases  were  found  elsewhere  (liver,  heart,  kidneys,  and 
spleen)  in  only  6.  The  cerebral  abscesses  were  multiple  in  13  and 
single  in  9  of  the  22  cases.  The  left  side  of  the  brain  was  alone  affected 
in  13  (7  single,  6  multiple).  In  a  large  proportion  of  the  cases  the  infec- 
tion is  carried  to  the  cortical  distribution  of  the  middle  cerebral  artery 
and  leads  to  the  complex  of  symptoms  known  as  cortical  or  Jacksonian 
epilepsy.  Hemiplegia  or  monoplegia  may  also  occur.  The  right  side 
of  the  body  is  more  often  affected.  In  some  instances  there  are  no 
symptoms  which  can  be  ascribed  to  cerebral  abscess. 

Diagnosis. — The  distinction  between  abscess  and  gangrene  in 
clinical  cases  rests  principally  on  the  uncertain  evidence  obtained  from 
the  odor  of  the  sputum. 

The  more  important  features  in  the  diagnosis  of  abscess  or  gangrene 
may  be  briefly  summarized.  The  history  may  be  suggestive.  Pul- 
monary destructive  lesions  may  follow  lobar  pneumonia,  the  inhala- 
tion of  foreign  bodies,  submersion,  etherization,  operation  about  the 
upper  respiratory  tract,  or  on  an  individual  known  to  be  the  subject 
of  bronchial  or  pulmonary  inflammation,  after  trauma  or  in  the  course 
of  suppuration  anywhere  in  the  body,  especially  in  the  pleura  or  abdo- 
men. The  general  symptoms  are  those  of  sepsis.  Cough  is  practically 
constant.  The  sputum  is  purulent.  In  typical  cases  there  may  be  the 
sudden  expectoration  of  a  large  amount  of  pus.  The  presence  in  the 
expectoration  of  shreds  of  pulmonary  tissue  or  elastic  tissue  with  an 
alveolar  arrangement  establishes  the  diagnosis. 

The  physical  signs  may  be  those  of  pulmonary  consolidation  and 
cavity  formation.  Only  the  signs  of  cavity  are  typical  of  abscess  and 
gangrene.    If  the  case  is  seen  when  there  is  a  circumscribed  collection 

1  Virchow's  Archiv,  1853,  Bd.  v,  p.  275. 

2  Guy's  Hosp.  Rep.,  1857,  S.  Ill,  vol.  iii. 

3  Deut.  Militararztl.  Zeitschrift,  1891. 

4  Deut.  Arch.  f.  klin.  Med.,  1884,  vol.  xxxiv. 

8  Guy's  Hosp.  Rep.,  vol.  lxi;   S.  Ill,  vol.  xlvi. 


304  DISEASES  OF  THE  LUNGS 

of  pus  within  the  substance  of  the  lung  and  before  a  communication 
is  established  with  the  bronchi  the  signs  are  like  those  over  centrally 
placed  fluid  due  to  other  causes.  If  air-holding  pulmonary  tissue 
intervenes  between  the  involved  region  and  the  chest  wall  there  is 
dulness  (not  flatness),  diminished  but  not  absent  breath  sounds,  voice, 
whisper  and  tactile  fremitus. 

The  more  frequent  location  of  areas  of  abscess  or  gangrene  in  the 
lower  lobes,  and  especially  the  right,  should  lead  to  the  examination 
(if  these  regions  with  special  care  in  suspected  cases,  but  in  the  absence 
of  physical  signs  indicating  the  position  of  the  process  no  reliance  can 
be  placed  on  its  probable  site  as  a  possible  point  for  surgical  inter- 
vention. The  lesions  are  usually  near  the  periphery  of  the  lung  and 
more  often  multiple  than  single.  Both  the  site  and  number  vary 
somewhat  with  the  cause,  and  a  careful  consideration  of  this  relation 
may  be  of  diagnostic  importance.  The  probability  of  multiple  lesions 
and  complicating  pulmonary  induration  increases  with  the  duration 
of  the  disease. 

A  determination  of  the  condition  of  the  pleura  is  of  special  import- 
ance. An  adherent  pleura  eliminates  one  source  of  danger  in  operative 
interference.  As  already  mentioned,  about  one-half  the  cases  of 
abscess  and  gangrene  coming  to  autopsy  at  the  Massachusetts  General 
Hospital  showed  adhesive  or  purulent  pleurisy  over  the  affected 
pulmonary  region.  A  previous  history  of  empyema  which  had  been 
opened  and  drained  would  indicate  with  practical  certainty  that  the 
pleural  space  was  obliterated.  Exceptions,  however,  have  been  noted 
in  rare  instances.  From  a  previous  history  of  fibrinous  or  serofibrinous 
pleurisy  no  certain  conclusions  can  be  drawn  as  to  the  condition  of  the 
pleura.  There  is,  of  course,  much  greater  chance  of  obliteration  of 
the  pleural  sac  than  in  an  individual  not  so  affected.  A  consideration 
of  the  cause  of  the  abscess  or  gangrene,  may  be  of  value.  Lobar  pneu- 
monia practically  always  involves  the  pleura.  When  the  disease 
follows  bronchopneumonia,  aspiration-pneumonia,  or  embolism,  the 
pleura  is  less  often  affected.  The  occurrence  of  pain  is  always  sugges- 
tive of  pleural  involvement  and  may  indicate  the  site  of  a  developing 
process.  Narrowing  of  the  intercostal  spaces  from  spasm  of  the  inter- 
costal muscles  may  be  an  important  early  sign.  More  than  normal 
inspiratory  retraction  of  the  intercostal  spaces  may  be  suggestive. 
Diminished  or  absent  pulmonary  excursion,  as  shown  by  percussion 
of  the  lower  pulmonary  margin  at  the  end  of  inspiration  and  expiration, 
may  furnish  valuable  evidence  concerning  the  condition  of  the  pleura. 
The  absence  of  the  diaphragm  shadow  on  the  affected  side  may  indi- 
cate an  adherent  pleura.  The  disappearance  of  pleural  friction  under 
observation  may  have  a  similar  value.  In  the  absence  of  more  definite 
and  typical  signs  of  thickened  pleura  or  pleural  effusion,  however, 
occasional  mistakes  in  the  diagnosis  of  pleural  involvement  are  inevit- 
able. The  surgeon,  therefore,  should  always  approach  the  pleura  as 
if  it  were  free  or  he  will  occasionally  create  artificial  pneumothorax 


PULMONARY  ABSCESS  AND  GANGRENE  305 

or  evacuate  a  pulmonary  abscess  or  gangrene  into  an  intact  pleura. 
An  artificial  empyema  will  then  add  to  the  gravity  of  an  already 
serious  condition. 

An  encysted  empyema  may  simulate  abscess  or  gangrene.  If  the 
pleurisy  is  primary,  cough  and  expectoration  may  be  insignificant 
or  absent.  Pain  is  likely  to  be  a  prominent  symptom  of  onset.  The 
sacculated  pleural  exudate  is  usually  bounded  on  one  side  by  the  thor- 
acic wall,  and  the  signs  are  those  of  pleural  fluid.  The  signs  of  uncom- 
plicated abscess  or  gangrene  are  those  of  pulmonary  consolidation 
and  cavity.  If  the  case  first  comes  under  observation  after  the 
empyema  has  ruptured  into  the  lung  and  communicates  freely  with 
the  bronchi,  the  signs  of  pyopneumothorax  may  be  present. 

Encapsulation  of  pus  between  the  lobes  of  the  lung  or  between  lung 
and  diaphragm  presents  special  difficulties  of  differentiation  from 
pulmonary  abscess  and  gangrene.  Interlobar  empyema  may  be  sug- 
gested by  a  position  corresponding  to  that  of  the  interlobar  septa  and 
the  absence  of  signs  above  and  below  this  region.  Encapsulation  of 
pus  between  lung  and  diaphragm,  without  contact  with  the  chest  wall, 
may  begin  with  the  symptoms  of  diaphragmatic  pleurisy.  Examina- 
tion may  disclose  the  process  several  inches  above  the  base  of  the 
lung. 

Perforation  of  the  lung  may  be  the  first  objective  sign  both  of  inter- 
lobar and  diaphragmatic  empyema.  The  gross  character  of  the  sputum 
is  seldom  of  much  assistance  in  the  diagnosis.  The  finding  of  elastic 
tissue,  with  an  alveolar  arrangement,  is  conclusive  evidence  of  pul- 
monary destruction,  but  does  not  exclude  a  complicating  empyema. 
The  presence  of  one  kind  of  bacteria  in  the  expectorated  pus  such  as 
the  pneumococcus  or  streptococcus  is  rather  in  favor  of  ruptured 
empyema  than  abscess  or  gangrene,  in  which  mixed  infection  is  more 
common. 

Involvement  of  the  pleura  early  in  the  course  of  abscess  or  gangrene 
may  suggest  a  primary  pleurisy  rather  than  pulmonary  disease.  The 
odor  of  the  sputum  or  the  breath  and  the  presence  of  elastic  tissue 
in  the  expectoration  may  suggest  the  diagnosis. 

The  differential  diagnosis  between  chronic  abscess  and  bronchiectasis 
can  hardly  be  made.  The  two  processes  are  usually  combined  and  thus 
in  the  presence  of  one  the  other  may  be  suspected. 

Pulmonary  tuberculosis  must  always  be  considered  in  the  presence 
of  abscess  or  gangrene.  It  is  more  likely  to  be  a  cause  when  the  pul- 
monary disease  appears  to  be  primary  rather  than  in  cases  obviously 
secondary  to  pulmonary  or  other  disease.  A  family  history  of  tuber- 
culosis or  opportunity  for  contagion,  a  history  of  hemoptysis  early 
in  the  course  of  an  apparently  mild  pulmonary  affection,  progressive 
loss  of  flesh  and  strength,  and  evening  rise  of  temperature  preceding 
the  onset  of  abscess  or  gangrene,  are  especially  suggestive  of  tubercu- 
losis. Tuberculous  processes  are  more  often  at  the  apex  than  at  the 
base  of  the  lung.  Hemoptysis  is  a  frequent  symptom  in  the  course  of 
20 


306 


DISEASES  OF  THE  LUNGS 


non-tuberculous  abscess  or  gangrene,  and  cannot  be  regarded  as 
specially  suggestive  of  tuberculosis  in  the  presence  of  destructive 
lesions  which  may  come  from  other  causes.  The  location  of  the  process 
is  merely  one  of  many  factors  to  be  taken  into  consideration  in  weigh- 
ing the  possibility  of  tuberculosis.  Non-tuberculous  as  well  as  tuber- 
culous destructive  lesions  may  occur  at  the  apex.  In  1905, 1  reported 
4  cases1  in  which  cavities  were  found  at  autopsy  in  the  superior  lobes 
of  the  lung,  but  without  gross  or  microscopic  evidence  of  tuberculosis. 
On  the  other  hand  tuberculous  lesions  are  not  very  infrequent  at  the 


Fig.  44 


Pulmonary  abscess. 


Dense  shadow  at  base  of  right  lung  in  cardiophrenic 
angle.     (No.  191,543.) 


bases.  Repeated  negative  examinations  of  the  sputum  do  not  posi- 
tively exclude  tuberculosis.  A  pulmonary  destructive  process  which 
has  progressed  to  the  stage  of  producing  an  abundant  purulent  sputum 
containing  elastic  tissue,  however,  and  fails  to  show  tubercle  bacilli 
after  diligent  and  repeated  search,  is  not  likely  to  be  tuberculous  in 
origin.  In  the  more  subacute  or  chronic  and  afebrile  cases,  the  sub- 
cutaneous use  of  tuberculin  in  ascending  doses  up  to  and  including 
10  mg.  may  be  used  as  a  final  resort  in  diagnosis. 
The  occasional  presence  of  so-called  pseudotubercle  bacilli  in  the 


1  Boston  Med.  and  Surg.  Jour.,  May  11  and  IS,  1905. 


PULMONARY  ABSCESS  AND  GANGRENE 


307 


sputum  from  cases  of  abscess  or  gangrene  demands  a  careful  study  of 
doubtful  organisms.  This  group  is  considered  elsewhere.  No  exami- 
nation of  the  sputum  from  cases  of  abscess  or  gangrene  is  complete 
without  a  search  for  actinomyces. 


Fig.  45 


Pulmonary  abscess.     Lodgment  of  fishbone  in  esophagus  four  weeks  ago.    Dense  shadow 
in  region  of  root  of  right  lung.     Foul  sputum  containing  elastic  tissue.    (No.  192,934.) 

X-ray  Examination. — This  may  confirm  the  results  of  physical  exami- 
nation, disclose  the  presence  of  multiple  areas,  only  one  of  which  has 
been  detected,  or  locate  a  focus  not  otherwise  to  be  found.  Lenhartz1 
states  that  the  arrays  first  disclosed  the  site  of  the  disease  in  about 
ten  of  his  cases  and  led  to  operative  interference.  The  .r-ray  plate 
is  an  important  guide  to  the  surgeon  if  operation  is  undertaken.  An 
area  of  abscess  or  gangrene  is  usually  seen  as  a  dense  shadow.  Its 
extent  is  always  greater  than  that  of  the  destructive  lesion  from  the 
constant  presence  of  inflammatory  changes  in  the  surrounding  tissue. 
In  rare  instances  an  empty  cavity  may  appear  as  a  relatively  less  dense 
shadow  within  the  involved  region.  Careful  comparison  of  the  physical 
findings  with  the  .r-ray  plate  assists  in  the  interpretation  of  the  latter. 
The  r-ray s  in  conjunction  with  the  history  and  physical  signs  may  make 
it  possible  to  differentiate  an  encapsulated  empyema  from  pulmonary 

1  Verhandl.  d.  Deut.  Rontgengesellschaft,  Bd.  i,  p.  55  u.  ff. 


308  DISEASES  OF  THE  LUNGS 

abscess  or  gangrene.  An  otherwise  doubtful  etiology  may  be  estab- 
lished as  in  a  case  soon  with  Dr.  J.  S.  Stone.  The  shadow  of  a  tack, 
thought  to  have  been  swallowed  five  years  before,  was  disclosed. 

Exploratory  Puncture. — The  diagnosis  of  abscess  or  gangrene  has 
often  been  made  in  this  way.  The  procedure  may  lead  to  an  erroneous 
diagnosis  or  to  dangerous  and  even  fatal  consequences.  It  is  an  unjus- 
tifiable method  and  cannot  be  too  strongly  condemned.  Exploration 
may  result  in  a  dry  tap  if  the  operator  fails  to  find  the  cavity  with 
the  aspirator.  The  cavity  may  be  reached,  but  its  contents  may  be 
too  viscid  to  flow.  Removal  of  the  purulent  contents  of  a  bronchus 
may  be  regarded  as  the  contents  of  a  cavity.  The  withdrawal  of  an 
infected  instrument  through  an  uninfected  pleura  may  lead  to 
empyema.  A  troublesome  superficial  abscess  may  follow  infection  of 
the  soft  parts.  Injured  bloodvessels,  lining  the  wall  or  traversing  the 
lumen  of  pulmonary  cavities  or  fresh  granulations  have  been  the  source 
of  fatal  bleeding.  Exploratory  incision  is  a  safer  procedure  in  cases  in 
which  abscess  or  gangrene  is  suspected.  Exploratory  puncture  of  an 
adherent  pleura  after  thoracotomy  is  performed  is  a  useful  means  of 
diagnosis  and  is  described  under  Treatment  (p.  314). 

Prognosis. — This  is  difficult  to  estimate  in  individual  cases.  Com- 
plete recovery  may  spontaneously  occur  both  in  abscess  and  gangrene. 
The  greater  frequency  of  abscess  at  autopsy  on  cases  of  lobar  or  bron- 
chopneumonia than  might  be  expected  from  their  clinical  course,  as 
already  mentioned,  suggests  that  the  repair  of  small  losses  of  pulmonary 
substance  is  often  effected.  Small  single  or  multiple  abscesses  are 
probably  frequently  overlooked  in  clinical  cases.  In  severe  and  pro- 
longed diffuse  or  localized  bronchitis,  without  signs  of  pulmonary 
involvement,  elastic  tissue  may  occasionally  be  found  in  the  sputum, 
and  yet  the  case  may  finally  end  in  complete  recovery.  In  one  of  the 
hospital  series,  with  an  acute  onset  of  cough  following  a  cold,  as  much 
as  an  ounce  of  purulent  sputum  mixed  with  blood  and  containing  elastic- 
tissue,  was  raised  at  each  paroxysm  of  cough.  There  were  signs  of 
pulmonary  consolidation  over  an  area  the  size  of  the  palm  below  the 
angle  of  the  left  scapula,  but  no  cavity  was  detected.  The  patient 
was  discharged  well  after  a  stay  of  two  months  in  the  hospital,  and 
when  seen  four  years  after  the  attack  there  were  no  symptoms  or  signs 
of  the  previous  trouble.  Anders  and  Pfahler1  report  an  instance  of 
complete  recovery  in  a  case  with  cavity  at  the  angle  of  the  right  scapula. 
The  sputum  contained  elastic  tissue.  Rieder2  made  a  diagnosis  of 
pulmonary  abscess  in  2  cases  by  means  of  the  .r-rays.  Elastic  tissue 
was  found  in  1.    Both  recovered.    Strauss3  reports  similar  cases. 

Laennec,4  Leyden,5  Wasmer,6  and  Kausch7  have  reported  sponta- 

1  Pennsylvania  Med.  Jour.,  1905-06,  ix,  425-427. 

2  Miinch.  med.  Woch.,  April  24,  1906.  3  Berl.  klin.  Woch.,  1913,  i,  509. 
4  Laennec  on  the  Chest,  Trans,  from  3d  French  ed.  Johns  Forbes,  1838. 

6  Volkmann's  klin.  Vortrage,    1st  S.,  No.  26,  p.  210. 

6  Uebcr  Spontanheilung  von  Lungenabscess  und  Lungengangran  Inaug.,  Diss.  Kiel., 
1903. 

7  Verhandl.  d.  Berliner  med.  Gesellsch.,  1912,  xliii,  77. 


PULMONARY  ABSCESS  AND  GANGRENE  309 

neous  recovery  from  pulmonary  gangrene.  Of  Leyden's  8  cases  of 
pulmonary  gangrene,  6  were  discharged  well,  1  left  the  hospital  with 
a  putrid  cavity,  and  the  last  was  still  in  the  hospital  at  the  date  of 
writing.  Wasmer  reports  4  cases  of  abscess  and  2  of  gangrene,  which 
he  regards  as  spontaneously  cured.  Elastic  tissue  or  shreds  of  lung 
substance  were  demonstrated  in  5  of  the  series.  A  survey  of  his  table 
shows  that  recovery  appears  to  have  been  complete,  as  judged  by  the 
absence  of  sputum  in  2,  one  of  whom  had  had  evident  signs  of  cavity, 
the  other  of  gangrene. 

Incomplete  recovery  is  commonly  observed.  The  acute  attack 
subsides,  but  the  patient  continues  to  cough  and  raise  abundant 
purulent  sputum.  Chronic  multiple  abscesses,  bronchiectasis  and 
interstitial  pneumonia  may  remain  as  the  result  of  an  acute  abscess 
or  gangrene.  In  the  chronic  stage,  the  patient  is  liable  to  recurrent 
attacks  of  bronchopneumonia  and  the  loss  of  more  pulmonary  sub- 
stance from  abscess  or  gangrene. 

In  general,  various  factors  influence  the  prognosis  of  abscess  and 
gangrene.  They  are,  unfortunately,  of  only  very  limited  value  in 
estimating  the  chances  of  the  individual  case.  The  prognosis  of  abscess 
is  much  more  favorable  than  that  of  gangrene. 

The  etiology  has  a  bearing  on  the  outcome.  Destructive  lesions 
following  trauma  and  lobar  pneumonia  appear  to  be  relatively  favor- 
able. In  the  case  of  trauma  this  is  due  to  the  development  of  suppura- 
tion in  previously  healthy  tissue  capable  of  repair.  With  lobar  pneu- 
monia the  single  or  circumscribed  nature  of  the  process  and  the  short 
viability  of  the  pneumococcus  may  be  of  importance.  An  origin  in 
bronchopneumonia  is  less  promising.  The  lesions  are  more  likely  to 
be  multiple  and  due  to  a  variety  of  organisms.  I  have  never  seen  any 
convincing  arguments  in  support  of  the  prevalent  belief  that  the  course 
of  abscess  due  to  the  influenza  bacillus  is  especially  unfavorable.  This 
organism  is  to  be  found  in  a  large  proportion  of  all  respiratory  lesions, 
both  benign  and  malignant.  Solid  foreign  bodies,  not  immediately 
removed  from  the  bronchi,  are  likely  to  give  rise  to  severe  disturbances 
and  an  almost  invariable  chronic  course.  Abscess  or  gangrene  arising 
as  a  complication  of  putrid  bronchitis  or  bronchiectasis  and  develop- 
ing in  indurated  tissue  is  usually  severe  and  long  continued.  The 
prognosis  of  abscess  or  gangrene  following  the  extension  of  suppura- 
tion from  neighboring  regions,  or  the  aspiration  of  fluid  material  varies 
with  the  amount  and  quality  of  the  fluid,  the  development  of  single 
or  multiple  areas,  the  previous  state  of  the  lung,  and  the  general  con- 
dition of  the  patient.  Such  processes  are  in  general  severe.  Metas- 
tatic pulmonary  abscess  or  gangrene,  as  a  pyemic  manifestation,  is 
likely  to  run  a  severe  and  fatal  course. 

The  prognosis  is  better  with  single  or  circumscribed  than  with  mul- 
tiple and  widely  distributed  processes.  Apical  localization  may  be 
more  favorable  if  the  relation  with  the  bronchi  is  such  that  gravity 
can  assist  in  the  evacuation  of  pus.    The  size  and  number  of  the  foci 


310  DISEASES  OF  THE  LUNGS 

must  also  be  taken  into  account  in  estimating  the  gravity  of  the  situa- 
tion. The  occurrence  of  complications  may  be  of  greater  significance 
than  the  original  process.  An  hemoptysis  or  cerebral  abscess  may  prove 
fatal.  Perforation  of  the  pleura  is  of  itself  a  serious  event,  but  may 
lead  to  early  detection  and  evacuation  by  operation. 

The  clinical  aspect  is  important  above  all  else  in  estimating  indi- 
vidual chances.  The  general  appearance  of  the  patient  and  the  degree 
of  sepsis  as  indicated  by  the  fever,  pulse,  sweats,  and  chills,  are 
valuable  guides.  Careful  observation  for  a  time,  with  a  record  of  the 
daily  amount  of  sputum,  may  furnish  important  data  for  the  estima- 
tion of  progress.  A  persistence  of  septic  symptoms  with  an  increasing 
amount  of  sputum  and  elastic  tissue  indicates  an  advancing  lesion. 
The  duration  has  an  important  bearing  on  the  outcome.  If  an  active 
process  has  existed  for  as  long  as  six  to  eight  weeks,  the  presence  of 
irreparable  pulmonary  damage  is  to  be  feared.  Multiple  lesions, 
bronchiectasis  and  pulmonary  induration  are  then  almost  inevitable. 

Mortality. — The  mortality  of  abscess  without  operation  cannot  be 
accurately  indicated.  That  of  gangrene  is  also  uncertain.  It  is  said 
by  Verneuill1  to  be  80  per  cent.  Lenhartz2  referred  to  the  statistics  of 
three  large  municipal  hospitals  in  Berlin  from  which  exact  figures 
concerning  pulmonary  gangrene  were  available.  The  mortality  was 
not  below  57  per  cent.,  and  for  the  most  part  rose  over  70  per  cent. 
Many  of  the  recovered  cases  have  persistent  cough  and  expectoration. 

Baron3  collected  seven  cases  of  abscess  in  infants.  The  disease  was 
fatal  in  all.  He  adds  one  case  with  recovery  after  evacuation  of  the 
abscess  cavity  by  operation. 

The  surgical  mortality  of  abscess  and  gangrene,  in  collected  cases, 
is  given  by  Garre4  as  follows : 

Abscess 182  cases;         Cured,  148;  Died,  34;  (18.5  per  cent.) 

Gangrene      .      ...      281      "  "        197;  "      84;  (29.3    "       " 

The  experience  of  individual  operators  is  of  greater  value.  Len- 
hartz,5 acting  in  the  double  capacity  of  internist  and  surgeon,  had 
operated  on  85  cases  of  pulmonary  gangrene  in  the  ten  years  preceding 
1907.  Of  this  number  53  were  cured  and  32  died.  If  4  cases  with 
tuberculosis  and  12  in  poor  general  condition  be  excluded  the  results 
are  more  favorable.  Of  69  cases,  53  (76.8  per  cent.)  recovered  and 
16  (23  per  cent.)  died.  Among  the  cured  cases  a  large  number  would 
have  died  without  operation.  Korte6  has  performed  pneumotomy 
on  28  patients  with  pulmonary  gangrene  or  abscess.  Of  this  number 
20  recovered  and  8  (28.5  per  cent.)  died. 

1  Ann.  de  la  Soc.  Beige  de  Chir.,  1900,  viii,  148. 

2  Verhandl.  d.  Deut.  Rontgengesellschaft,  1905,  i,  56. 

3  Ueber  Lungenabscess  bei  Siiuglingen,  Berl.  klin.  Woch.,  January  20,  1908. 

4  Garre  and  Quincke.  Lungenchirurgie  2  aufl.,  1912,  p.  127. 
6  Verhandl.  d.  Deut.  Gesellschaft  f.  Chir.,  1907,  xxxvi,  60. 

6  Arch.  f.  klin.  Chir.,  1908,  Ixxxv,  2. 


PULMONARY  ABSCESS  AND  GANGRENE  311 

An  important  difference  in  the  results  of  operation  exists  between 
acute  and  chronic  cases.  This  is  strikingly  indicated  in  11  operated 
cases  at  the  Massachusetts  General  Hospital.1  Of  6  cases  of  abscess 
or  gangrene  (3  abscess,  1  gangrene,  and  2  either  abscess  or  gangrene) 
operated  within  three  weeks  to  two  months  of  onset  5  showed  imme- 
diate improvement  and  were  later  discharged  relieved;  3  were  in  per- 
fect health  after  four  to  twelve  years;  2  could  not  be  traced;  1  died 
soon  after  operation  and  multiple  abscesses  were  found  at  autopsy. 
Of  5  cases  of  abscess  or  gangrene  (3  abscess  and  2  either  abscess  or 
gangrene),  with  symptoms  for  from  nine  months  to  four  years,  3  died 
soon  after  operation,  1  failed  to  be  relieved  after  several  operations, 
and  the  last  case  recovered. 

Treatment. — (1)  Medical. — In  the  acute  cases  the  patient  should 
be  abed  and  remain  there  as  long  as  there  is  fever  or  foul  expectoration. 
Means  similar  to  those  for  pulmonary  tuberculosis  should  be  insti- 
tuted to  improve  the  general  condition.  The  food  should  be  abundant 
and  easily  digestible.  Extra  feedings  are  to  be  advised,  if  they  can 
be  taken.  An  abundance  of  fresh  air,  by  night  as  well  as  by  day,  will 
help.  If  treatment  is  carried  out  indoors  a  large  sunny  room  should 
be  chosen  and  the  windows  kept  open  constantly.  Free  ventilation 
lessens  the  effect  of  an  offensive  expectoration  on  the  patient  and  the 
attendants. 

The  patient  must  be  cautioned  not  to  swallow  the  sputum.  This 
should  not  be  expectorated  into  cloths  or  handkerchiefs,  but  into  a 
special  receptacle.  Care  should  be  taken  not  to  soil  the  beard  or 
clothing.  The  sputum  cup  should  be  emptied  as  frequently  as  pos- 
sible. A  mouth  wash  may  be  used  at  regular  intervals  and  also  after 
each  paroxysm  of  cough. 

An  effort  should  be  made  to  favor  the  evacuation  of  pus  by  position. 
The  patient  may  instinctively  assume  the  most  favorable  posture.  If 
the  disease  is  in  the  lower  lobes,  evacuation  may  be  favored  if  the 
patient  lowers  his  head  over  the  edge  of  the  bed  during  the  paroxysm 
of  cough.  At  intervals,  during  the  day,  the  patient  may  lie  with  the 
affected  side  uppermost,  in  an  effort  to  drain  the  pus  into  the  trachea. 
Elevation  of  the  foot  of  the  bed,  on  which  the  patient  lies  at  full  length 
on  the  back  or  abdomen,  may  also  be  tried.  Quincke2  has  specially 
emphasized  position  in  the  treatment  of  bronchiectasis.  Franker3  has 
had  an  adjustable  bed  frame  constructed  by  means  of  which  the  patient 
can  be  placed  in  any  desired  position. 

No  reliance  can  be  placed  on  drugs  in  the  treatment  of  abscess  or 
gangrene.  An  effort  to  check  the  cough,  if  successful,  may  aggravate 
the  condition  by  increasing  the  retention  of  pus.  The  use  of  narcotics 
should  be  restricted  to  the  relief  of  a  dry  and  harassing  cough,  which 

1  Lord.  Internat.  Clinics,  1906,  vol.  ii,  16th  S.  Scudder  (Bost.  Med.  and  Surg.  Jour., 
October  1,  1914)  has  collected  16  subsequent  cases  at  the  Massachusetts  General  Hos- 
pital, of  whom  5  died,  3  were  unimproved,  and  8  were  relieved  or  cured. 

2  Berl.  klin.  Woch.,  1898,  No.  24,  p.  525. 

3  Spez.  Path.  u.  Ther.  d.  Lungenkrankheiten,  1904,  p.  566. 


312  DISK  asks  OF  THE  LUNGS 

prevents  sleep  or  exhausts  the  patient.  Such  derivatives  of  opium 
as  morphin,  gr.  %  (0.008  gm.),  codein,  gr.  .*  (0.032  gm.),  or  heroin, 
gr.  jV  (0.0054  gm.),  may  then  be  used  and  preferably  only  at  night. 
Various  expectorants  may  be  tried.  Ammonium  chloride,  gr.  10  (0.65 
gm.),  or  the  inhalations  of  simple  or  medicated  warm  vapor  may  be 
useful.  For  the  offensive  odor  of  the  sputum  and  breath,  oil  of 
turpentine,  oil  of  eucalyptus,  or  myrtol  in  doses  of  3  to  5  drops,  in 
gelatin  capsules  or  in  milk,  is  recommended.  Injections  into  the  site 
of  the  pulmonary  lesions  cannot  be  advised. 

2.  Surgical. — Indications  for  Operation. — Acute  Cases. — Acute  pul- 
monary abscess  and  gangrene  are  surgical  affections.  The  best  results 
can  be  expected  only  when  the  physician  and  surgeon  work  together. 
The  site  of  the  process  must  be  known.  No  reliance  can  be  placed  on 
its  probable  position  as  a  possible  point  of  attack.  The  chances  of 
success  are  infinitely  better  when  the  process  is  single,  but  multiple 
areas  are  not  necessarily  a  contra-indication.  The  assistance  of  the 
x-rays  in  determining  the  site  and  single  character  of  the  process  is 
almost  indispensable.  It  must  be  constantly  in  mind  that  the  chances 
of  cure  diminish  writh  the  lapse  of  time. 

Spontaneous  and  complete  recovery  occurs  both  in  abscess  and 
gangrene,  and  the  attendant's  judgment  will  often  be  taxed  to  its 
utmost  to  decide  whether  an  expectant  policy  or  operation  is  the  wisest 
course.  The  knowledge  that  in  many  of  the  recovered  cases  there  is 
permanent  and  distressing  pulmonary  damage  may  influence  the 
decision.  Lobar  pneumonia  as  a  cause  may  be  considered  of  favorable 
moment  in  estimating  the  probable  outcome.  The  clinical  features 
are  of  more  importance. 

In  the  presence  of  a  small  process,  without  marked  symptoms  of 
sepsis,  a  pure,  purulent  sputum  (not  foul)  and  without  a  large  amount 
of  lung  tissue,  an  expectant  policy  may  be  followed.  An  estimate  of 
progress  may  be  made  from  the  amount  and  character  of  the  sputum 
and  the  temperature  chart.  If  recovery  or  marked  improvement  does 
not  occur  wTithin  three  to  four  weeks,  operation  should  be  considered.- 
Operation  is  indicated,  on  the  other  hand,  in  the  presence  of  a  large 
cavity,  marked  sepsis,  putrid  sputum  and  abundant  lung  shreds. 
If  empyema  is  present  in  any  case  it  should  be  opened  and  drained. 
An  accessible  abscess,  elsewhere,  which  has  invaded  the  lung  should 
also  be  opened. 

Multiple  areas  of  abscess  or  gangrene  may  usually  be  considered  a 
contra-indication  to  operation.  This  is  more  particularly  the  case 
when  the  lesions  are  widely  separated.  Multiple  and  circumscribed 
foci  may  be  successfully  operated,  in  acute  cases.  A  complicating 
cerebral  abscess  makes  operation  inadvisable.  Hemoptysis  is  not 
necessarily  a  contra-indication.  If  recent  there  is,  of  course,  the  danger 
of  inducing  a  second  attack  by  the  manipulations  of  the  lung.  This  may 
also  occur  spontaneously  and  end  fatally.  Much  depends  on  the 
certainty  with  which  the  site  of  the  bleeding  can  be  found.  The 
absence  of  pleural  adhesions  is  not  a  contra-indication. 


PULMONARY  ABSCESS  AND  GANGRENE  313 

Chronic  Cases. — The  exigencies  of  the  individual  case  determine 
the  propriety  of  surgical  intervention  in  cases  which  have  lasted  tor 
months  or  years.  In  general,  operation  is  not  to  be  advised.  The 
chances  are  much  in  favor  of  a  multiple  even  though  circumscribed 
process.  Induration  of  the  affected  region  may  prevent  the  closure 
of  the  cavity.  More  extensive  costatectomy,  pneumolysis,  and 
pulmonary  resection  rather  than  simple  incision  are  then  likely  to 
be  necessary.  There  is  greater  danger  of  hemorrhage.  The  chance 
of  aspiration-pneumonia  during  prolonged  narcosis  increases  the  oper- 
ative risk.  The  likelihood  of  effecting  a  cure  is  also  far  less  favorable. 
(See  Bronchiectasis.) 

A  careful  history  of  the  case  may  indicate  that  the  destructive 
pulmonary  process  in  question  is  of  more  recent  origin  than  might  other- 
wise be  supposed,  and  hence  more  favorable  for  operation.  If  situated 
in  normal  lung  tissue,  the  situation  may  be  little  different  from  that 
in  an  uncomplicated  and  acute  case.  In  the  subacute  and  chronic- 
cases  I  believe  that  a  progressive  lesion  affords  a  better  chance  for 
cure  than  one  in  which  the  disease  is  quiescent.  The  continued  pres- 
ence of  elastic  tissue  in  the  sputum  may  be  of  value  in  estimating  a 
progressive  character. 

Technic  of  Operation. — The  focus  of  abscess  or  gangrene  should 
be  as  nearly  as  possible  empty  before  operation  is  undertaken. 
The  patient  should  therefore  be  urged  to  cough  and  evacuate 
the  cavity.  An  attempt  should  also  be  made  to  assist  the  evacua- 
tion by  position.  Local  anesthesia  is  to  be  preferred,  especially 
for  patients  in  poor  condition  and  those  in  whom  an  abundance 
of  secretion  endangers  sound  parts  of  the  lung  by  aspiration.  Gen- 
eral anesthesia  must  often  be  used.  It  is  necessary  in  children  and 
nervous  individuals.  The  patient  should  be  only  lightly  anesthetized. 
Whether  local  or  general  narcosis  is  employed  the  patient  may  well 
be  given  morphin  subcutaneously  before  the  operation.  After  the 
operator  has  completed  the  pulmonary  incision  the  anesthetic  may 
be  removed,  as  the  pulmonary  pleura  and  lung  are  insensitive. 

The  position  of  the  patient  during  the  operation  is  of  importance. 
He  should  be  placed  so  that  the  affected  region  is  dependent,  the 
unaffected  lung  thus  being  given  full  play  and  the  danger  of  aspirating 
pus  minimized.  Korte1  recommends  a  slight  inclination  toward  the 
sound  side  for  operations  on  the  anterior  thorax.  When  operating 
on  the  lateral  or  posterior  regions  he  places  the  patient  on  the  sound 
side  in  the  full  lateral  position. 

Thoracotomy. — The  incision  should  be  made  over  the  site  of  the 
lesion  and  parallel  with  the  ribs.  The  soft  parts  are  retraced.  About 
6  cm.  of  two  or  more  ribs  are  subperiosteally  resected.  Inside  the 
ribs  and  intercostal  muscles  lies  the  thin  endothoracic  fascia  beyond 
which  is  the  costal  pleura. 

1  Arch.  f.  klin.  Chir.,  1908,  vol.  Ixxxv. 


314  DISEASES  OF  THE  LUNGS 

Plan-atomy. — Is  the  pulmonary  adherent  to  the  costal  pleura  or  free? 
It*  adherent,  the  operation  is  relatively  simple.  If  free,  it  may  be  very 
difficult.    The  respiratory  excursion  of  the  pulmonary  pleura  may  be 

plainly  visible  through  the  thin  partition  which,  remains  after  removal 
of  the  ribs.  Tlie  condition  of  the  pleura  may  be  doubtful.  Palpable 
induration  of  the  underlying  structures  suggests  an  obliteration 
of  the  pleural  sac  at  this  point,  but  it  is  easy  to  be  deceived  in  this 
matter.  Consolidated  pulmonary  tissue  may  give  the  same  feeling. 
To  be  sure,  the  pleura  is  likely  to  be  adherent  when  induration  is  present 
but  one  never  can  be  quite  certain.  Then,  too,  adhesions,  though 
present,  may  be  insecure  or  limited  to  a  small  area,  while  the  neigh- 
boring region  is  free.  In  all  cases,  therefore,  it  is  wisest  to  proceed  as 
if  the  pleural  sac  were  free. 

The  parietal  should  be  sutured  to  the  costal  pleura,  including  the 
lung  and  intercostal  muscles  (costopneumopexy).  A  continuous 
suture  with  a  round  and  curved  needle  is  used  and  each  stitch  locked 
by  introducing  the  needle  between  the  entrance  and  exit  of  the  preced- 
ing. The  field  of  operation  should  thus  be  enclosed.  If  the  pleura 
is  free,  such  fixation  cannot  be  relied  upon  with  certainty  to  prevent 
collapse  of  the  lung,  as  the  stitches  may  tear  away.  The  operator 
may  be  influenced  by  the  conditions  in  his  further  course.  If  delay 
is  dangerous  or  pleural  adhesions  are  present,  the  operation  may  be 
continued.  If  interference  is  not  urgent  or  the  condition  of  the  pleura 
doubtful,  it  is  best  to  perform  the  operation  in  two  stages,  waiting 
now  for  six  to  ten  days  in  the  hope  that  adhesions  will  form.  Silk 
is  probably  the  best  suture  material.  Medicated  suture  material 
(silk  soaked  in  turpentine  (Karewski),  juniper-iodoform  catgut  or 
iodine-catgut  (Korte)  )  has  been  recommended.  Many  other  methods, 
such  as  injections  (tincture  of  iodine,  mercuric  nitrate),  applications 
(zinc  chloride  paste,  iodoform  gauze),  cauterization,  or  electrolysis 
have  been  suggested,  but  have  never  come  into  general  use. 

Pnewnotomy. — Difficulty  may  be  experienced  in  finding  the  cavity. 
Palpation  may  disclose  an  indurated  area  with  a  central  depression. 
Exploratory  puncture  with  the  aspirating  needle  or  air-tight  trocar, 
contra-indicated  in  the  presence  of  an  unopened  throax  and  free  pleura, 
may  now  be  of  great  service.  Introduction  of  the  instrument  further 
than  2  to  3  cm.  into  the  lung  may  injure  important  vessels  and  cause 
dangerous  hemorrhage.  If  the  focus  is  not  at  first  discovered,  puncture 
should  be  made  in  other  nearby  places.  The  prevailing  peripheral 
site  of  abscess  and  gangrene  demands  a  careful  search  of  this  region 
before  a  deeper  location  is  suspected.  If  necessary  the  lung  tissue  may 
be  incised  to  a  depth  of  2  to  3  cm.  within  the  field  of  operation.  Failing 
in  this  a  blunt  instrument  may  be  introduced  to  a  greater  depth,  but 
not  without  danger.  If  pus  is  reached,  the  cavity  should  be  opened 
with  the  cautery  passed  alongside  the  instrument  with  which  it  was 
discovered.  The  knife  or  scissors  may  also  be  used,  but  the  cautery 
is  to  be  preferred,  especially  for  the  incision  of  hyperemic  tissue. 


PULMONARY  ABSCESS  AND  GANGRENE  315 

Lenhartz1  stated  that  sometimes  one  must  go  16  to  20  cm.  into  the  lung 
with  the  cautery  to  find  the  gangrenous  area.  If  pus  cannot  be  found 
the  wound  should  be  packed  in  the  hope  that,  as  sometimes  happens, 
it  may  later  drain  into  the  field  of  exploration. 

Pulmonary  tissue  overlying  an  area  of  abscess  or  gangrene  should  be 
freely  opened  to  secure  constant,  free  drainage.  The  contents  of  the 
cavity  should  be  absorbed  with  gauze  sponges,  pulmonary  arteries 
traversing  the  lumen  ligated  and  the  ends  of  open  bronchi  discharging 
pus  widened  with  a  blunt  instrument  or  cautery.  Korte2  recommends 
the  use  of  a  head-  or  cystoscope-lamp  for  illumination.  A  good-sized 
rubber  drainage  tube,  about  which  gauze  is  lightly  packed,  should 
reach  from  the  thoracic  surface  to  the  bottom  of  the  cavity.  Washing 
out  the  cavity  is  too  dangerous  to  recommend.  It  may  carry  infectious 
material  through  the  open  bronchi  into  sound  parts  of  the  lung. 
Lejars3  removed  a  large  sequestrum,  measuring  7x4x5  cm.,  from  a 
cavity  representing  the  right  upper  lobe.    The  patient  recovered. 

Pneumectomy. — Resection  of  a  lobe  of  the  lung  for  pulmonary  abscess 
was  successfully  performed  by  Krause.4    The  patient  recovered. 

Dangers  and  Accidents. — Partial  or  complete  pneumothorax  may 
occur  during  operation.  Sudden  collapse  of  the  lung  may  be  followed 
by  severe  dyspnea,  cardiac  weakness,  and  collapse.  Murphy5  has  shown 
that  the  cause  probably  lies  in  the  consequent  relaxation  and  oscilla- 
tion of  the  mediastinal  curtain,  the  fixation  of  which  with  forceps  or 
a  pull  on  the  collapsed  lung  serving  to  relieve  the  symptoms.  Geru- 
lanos6  has  demonstrated  that  collapse  more  often  follows  operative 
pneumothorax  on  the  right  than  on  the  left  side.  This  is  probably 
due  to  the  larger  size  of  the  right  lung.  The  accident  is  more  to  be 
feared  with  normal  lung  and  intact  mediastinum  than  in  the  presence 
of  pulmonary  or  pleural  disease  which  may  limit  the  collapse  of  the 
lung  and  the  elasticity  of  the  mediastinum.  Garre7  emphasizes  the 
important  relation  which  the  size  of  the  thoracic  opening  into  the  pleura 
bears  to  the  symptoms.  A  pleural  opening  smaller  than  the  glottis 
still  permits  even  the  fully  collapsed  lung  to  take  some  part  in  respira- 
tion. A  large  pleural  opening  not  only  excludes  the  collapsed  lung 
from  participation  in  the  respiratory  act,  but  greatly  embarrasses 
the  sound  lung.  Inspiration  is  followed  by  dislocation  of  the  medias- 
tinal curtain  toward  the  sound  side,  thus  limiting  pulmonary  inflation. 
Forced  expiration,  with  consequent  positive  intrathoracic  pressure 
on  the  sound  side,  dislocates  the  mediastinum  toward  the  diseased 
side  and  causes  insufficient  deflation. 

1  Lenhartz  and  Kissling,  Verhandl.  d.  Deut.  Rontgengesellschaft,  Bd.  i,  S.  55,  u.  ff. 

2  Loc.  cit. 

3  Bull,  et  mem.  Soc.  de  Chir.  de  Paris,  1911,  xxxvii,  749. 

4  Seit  11  Jahren  geheilter  Fall  von  Resektion  einer  Lungenlappens  bei  Lungenabszess, 
Munch,  med.  Woch.,  1911,  lviii,  2418. 

5  Jour.  Amer.  Med.  Assoc.,  July,  1898. 

6  Deut.  Aerzte  Zeit.,  1902,  Heft  9  und  10. 

7  Garre  and  Quincke.     Lungenchirurgie,  2  Aufi.,  1912,  p.  22. 


316  DISEASES  OF  THE   LUNGS 

The  pleural  sac  may  be  accidently  opened  during  the  removal  of  the 
rit)s  or  in  the  process  of  fixation  by  suture,  korte  then  attempts  to 
dose  the  defect  by  including  a  gauze  compress,  applied  to  the  affected 
region  in  a  wider  stitch  tied  over  the  gauze.     If  the  lung  collapses, 

it  should  be  quickly  grasped  with  the  dressing  forceps,  drawn  into  the 
pleural  opening  and  there  fixed  by  suture.  Artificial  pneumothorax 
occurred  in  six  of  Korte's  eases.  It  was  thus  remedied  and  was  not 
followed  by  unfavorable  results  which  could  be  ascribed  to  the  accident. 
A  small  amount  of  air  within  the  pleura  is  of  itself  harmless  and  is 
quickly  absorbed.  After  costatectomy  and  during  difficult  breathing 
the  lung  may  "flutter"  to  and  fro,  even  when  the  pleural  sac  is  oblit- 
erated. The  respiration  may  be  much  embarrassed.  Withdrawal  and 
fixation  of  the  lung  to  the  edges  of  the  incision  may  be  attempted. 
The  operation  may  need  to  be  discontinued.  In  one  of  Korte's  cases, 
death  during  a  second  operation  was  apparently  due  to  this  cause 

Empyema  may  follow  exploratory  puncture  or  pneumotomy,  when 
the  pleural  sac  is  free  or  incompletely  obliterated.  It  is  usually  asso- 
ciated with  partial  or  complete  pneumothorax  when  it  follows  opera- 
tion. It  is  a  dangerous  complication  and  must  be  carefully  guarded 
against,  but  may  occur  even  when  the  utmost  care  is  taken.  Lenhartz1 
lost  two  patients  from  empyema. 

Hemorrhage  may  occur  from  the  intercostal  or  pulmonary  arteries. 
It  is  especially  to  be  feared  during  exploratory  puncture  of  the  unopened 
thorax,  as  the  bleeding  vessel  may  then  be  inaccessible.  Capillary 
bleeding  may  be  controlled  by  the  cautery  or  tampon".  Arterial  bleed- 
ing may  be  stopped  by  securing  the  bleeding  point  with  hemostatic 
forceps  and  the  ligature.  Hemoptysis  may  occur  during  operation 
as  in  one  of  Korte's  cases,  with  a  bronchiectatic  cavity  of  the  upper 
lobe.  A  long  blood  clot,  lodged  in  the  larynx,  caused  severe  respiratory 
disturbance,  but  was  finally  removed  from  the  pharynx  without  the 
necessity  of  tracheotomy.  Air  embolism  may  follow  the  entrance  of 
air  into  veins  in  the  midst  of  indurated  tissue. 

Finally,  sudden  respiratory  disturbance,  collapse  and  death  during 
or  immediately  after  the  operation,  may  occur  in  uncomplicated  cases. 
Postmortem  examination  may  fail  to  disclose  the  cause.  Reflex 
cardiac  inhibition  is  a  probable  explanation. 

Results  of  Operation. — In  successful  cases  the  amount  of  sputum 
rapidly  diminishes.  The  foul  odor  to  the  breath  and  sputum  subside. 
The  appetite  improves.  The  fever  gradually  falls  to  normal.  Incom- 
plete recovery  may  be  due  to  bronchopneumonia,  multiple  cavities, 
or  a  complicating  pleurisy.  Complete  recovery  may  follow  the  opera- 
tive closure  of  even  large  losses  of  pulmonary  substance.  No  evidence 
of  the  previous  disease  may  be  disclosed  by  .r-ray  examination. 

Lenhartz2  reports  the  case  of  a  man,  aged  forty-nine  years,  in  whom 
a  fist-sized  gangrenous  cavity  of  the  right  lower  lobe  was  evacuated. 

1  Mitth.  a.  d.  Grenz.  d.  Med.  u.  Chir.,  Bd.  ix.  2  Loc.  cit. 


PULMONARY  ABSCESS  AND  GANGRENE  317 

Death  occurred  about  two  and  one-half  years  later  from  gastric  cancer. 
At  autopsy  thick  pleural  adhesions  were  the  only  evidence  of  the  pul- 
monary trouble. 

After-treatment. — This  is  usually  simple.  Impaired  drainage  may 
be  due  to  more  rapid  closure  of  the  thoracic  wound  than  of  the  pul- 
monary cavity.  It  is  well,  therefore,  to  pack  the  pulmonary  cavity 
loosely  with  gauze,  while  the  thoracic  wound  is  tightly  filled.  The 
drainage  tube  should  be  gradually  shortened  so  that  healing  will 
occur  from  within.  More  extensive  costatectomy  may  be  needed. 
A  complicating  empyema  may  have  to  be  opened.  Postoperative 
bleeding  occurred  in  two  of  Korte's  cases.  In  one,  ligature  of  a  bleed- 
ing vessel  in  the  incised  pulmonary  tissue  was  necessary  eight  days 
after  the  operation.  In  the  second  case,  a  fatal  arterial  hemorrhage 
occurred  twenty-one  days  after  operation.  At  autopsy,  a  small  aneu- 
rysmal dilatation  in  the  cavity  was  found  to  have  ruptured.  In  still 
another  patient  a  similar  accident  was  probably  prevented  by  the 
ligature  of  a  large  pulsating  vessel  in  the  gangrenous  cavity. 

Positive  and  Negative  Pressure  Apparatus. — Sauerbruch's  negative 
pressure  chamber,  Brauer's  positive  pressure  method  or  their  modifi- 
cation have  as  yet  been  applied  in  the  surgery  of  pulmonary  abscess  and 
gangrene  only  in  isolated  instances.  Their  use  would  not  obviate  the 
necessity  of  pleural  fixation.  They  would  greatly  lessen  the  danger 
of  pneumothorax  and  agitation  of  the  lung  from  forced  respiration 
during  the  operation.  Postoperative  pneumothorax  would  still  as 
readily  occur.  Positive  pressure  may  increase  the  danger  of  aspiration- 
pneumonia. 

Intratracheal  Insufflation. — Meltzer  and  Auer's1  method  consists  in 
the  introduction  deep  into  the  trachea  of  a  flexible  elastic  tube  of 
suitable  size.  A  nearly  constant  stream  of  air  is  driven  through  this 
tube  and  returns  by  way  of  the  space  between  the  tube  and  the 
walls  of  the  trachea.  The  danger  of  artificial  pneumothorax  in  the 
performance  of  thoracic  operations  is  overcome  by  this  means,  since 
the  process  of  ventilation  can  be  efficiently  carried  on  without  any 
aid  of  the  respiratory  mechanism.  The  method  is  simple,  has  proved 
satisfactory,  and  may  be  used  in  cases  in  which  there  is  danger  of 
pneumothorax  during  thoracic  operations.  If  desired,  insufflation 
anesthesia,  also,  may  be  used. 

Artificial  Pneumothorax. — Forlanini2  treated  a  case  of  putrid  pul- 
monary abscess  of  the  right  lung  secondary  to  croupous  pneumonia 
by  means  of  artificial  pneumothorax.  The  abscess  had  lasted  almost 
six  years.  The  patient  was  practically  well  at  the  time  of  the  last 
report  three  years  after  treatment  was  begun. 

1  Jour.  Exp.  Med.,  1909,  xi,  622;  see  also  Meltzer,  Jour.  Amer.  Med.  Assoc,  August 
12,  1911. 

2  Munch,  med.  Woch.,  January  18,  1910. 


CHAPTER  XVII. 
CIRCULATORY  DISTURBANCES. 

Pulmonary  Congestion. — In  the  lungs,  as  elsewhere,  active  and 
passive  congestion  may  be  considered.  The  two  forms  are  not  infre- 
quently combined  and  sharp  distinctions  between  them  cannot  be 
made.  Both  soon  lead  to  the  escape  of  fluid  from  the  pulmonary 
vessels. 

Active  Congestion  (Active  Hyperemia). — Engorgement  of  the  pul- 
monary vessels  with  an  increased  amount  of  arterial  blood  occurs 
in  the  initial  stage  of  all  inflammations  of  the  lung,  such  as  pneu- 
monia, tuberculosis,  and  pleurisy.  A  zone  of  hyperemia  likewise 
surrounds  all  circumscribed  inflammatory  pulmonary  lesions.  Inflam- 
matory hyperemia  too  slight  in  degree  to  be  termed  pneumonia 
may  be  seen  in  the  course  of  influenza  and  in  typhoid  fever.  The 
inhalation  of  irritating  substances  may  also  be  a  cause.  In  the  presence 
of  an  intrathoracic  lesion  such  as  pneumonia  or  a  pleural  effusion 
which  limits  the  pulmonary  space,  the  pulmonary  vessels  outside  the 
affected  region  may  be  overdistended  as  a  compensatory  process. 
This  collateral  hyperemia  or  fluxion,  as  it  is  called,  is  of  little  if  any 
importance.  Pulmonary  congestion  accompanying  malaria  has  been 
ascribed  to  the  malarial  plasmodia,  and  is  said  to  appear  during  the 
febrile  period  and  to  disappear  during  the  intervals  of  apyrexia. 
Although  pulmonary  congestion  associated  with  malaria  may  be 
aggravated  during  the  paroxysms,  the  malarial  origin  of  the  conges- 
tion itself  is  doubtful. 

French  writers  recognize  a  primary  and  independent  pulmonary 
congestion  under  the  name  of  Woillez's  disease.  There  may  be  an 
initial  chilliness,  rapid  rise  of  temperature,  pain  in  the  side,  and  cough 
with  mucoid  or  mucopurulent  but  not  rusty  sputum.  On  physical 
examination  there  is  slight  dulness,  diminished  tactile  fremitus, 
diminished  breathing  with  prolonged  expiration  and  subcrepitant  or 
moist  rales.  The  disease  lasts  only  four  to  five  days,  defervescence 
occurring  by  lysis.  The  outcome  is  almost  invariably  favorable. 
The  condition  has  been  specially  studied  by  Carriere,1  who  demon- 
strated pneumococci  alone,  or  more  often  mixed  with  other  organisms 
in  the  sputum  in  9  of  14  cases.  Pneumococci  were  also  found  in 
material  obtained  by  lung  puncture  in  8  of  10  cases.  Inoculation 
of  rabbits  seemed  to  indicate  that  the  organism  waa  of  attenuated 
virulence.      The    disease    does    not    present    sufficiently    distinctive 

1  Revue  de  rued.,  1898,  pp.  765  and  951;   and  1899,  p.  54. 


CIRCULATORY  DISTURBANCES  319 

characters  to  justify  its  inclusion  as  a  special  form  of  pulmonary 
congestion  and  seems  rather  to  be  an  abortive  pneumonia. 

Hyperemic  parts  of  the  lung  are  dark  red  in  color,  of  increased 
volume,  more  resistant  and  less  elastic  than  normal.  The  cut  surface 
exudes  an  increased  amount  of  dark  red  fluid.  The  tissue  is  still 
air  holding.  The  whole  lung  is  rarely  affected.  The  dependent  parts 
are  most  often  the  site  of  the  process. 

On  microscopic  examination,  the  pulmonary  capillaries  are  found 
engorged  with  blood.  The  alveolar  spaces  contain  serum,  desquamated 
epithelium,  and  a  few  mononuclear  and  polynuclear  leukocytes. 

Simple  congestion  may  give  rise  to  dyspnea.  Physical  signs  are 
lacking  unless  the  congestion  is  accompanied  by  exudation.  Rales 
may  then  be  heard  over  the  affected  region. 

Active  congestion  of  the  lung  hardly  deserves  consideration  apart 
from  the  diseases  to  which  it  is  secondary.  The  outlook  and  treat- 
ment are  those  of  the  underlying  conditions. 

Passive  Congestion. — This  arises  in  consequence  of  obstruction  to 
the  return  of  blood  from  the  lungs  to  the  heart.  It  is  most  often 
cardiac  in  origin,  and  due  to  disease  of  the  mitral  valve  or  insufficiency 
of  the  left  ventricle.  The  passive  congestion  is  especially  marked  in 
long-standing  cases  of  mitral  stenosis  with  hypertrophy  of  the  right 
ventricle.  In  this  condition,  blood  is  strongly  forced  into  the  pul- 
monary circuit  already  overfilled  because  of  the  impeded  outflow 
through  the  mitral  valve.  When  in  consequence  of  aortic  valve  disease, 
arteriosclerosis  or  chronic  nephritis,  a  left  ventricle  previously  capable 
of  carrying  on  the  circulation  begins  to  give  way,  pulmonary  conges- 
tion also  arises.  Although  the  lungs  are  the  first  to  feel  the  effect  of 
the  stasis,  yet  in  the  absence  of  hypertrophy  of  the  right  ventricle, 
the  lungs  suffer  far  less  than  in  mitral  stenosis.  The  congestion  is 
distributed  beyond  them  to  the  right  auricle  and  the  systemic  veins, 
thus  relieving  the  lungs  of  a  part  of  the  burden.  Compression  of  the 
pulmonary  veins  from  intrathoracic  tumors  or  thrombosis  of  the 
pulmonary  veins  may  also  be  a  cause. 

Brown  Induration. — In  the  most  extreme  grade  of  passive  congestion 
as  seen  in  long-standing  cases  of  mitral  disease,  the  lungs  are  volumi- 
nous, heavier  than  normal,  firm  and  inelastic,  and  cut  or  tear  with 
resistance.  The  color  is  brownish  or  russet  brown,  due  to  the  increased 
amount  of  blood  and  the  deposit  of  blood  pigment  in  the  interstitial 
tissue  and  the  alveolar  cells.  Small  parenchymatous  hemorrhages 
may  give  to  the  tissue  an  uneven  coloring.  The  bloodvessels  of  the 
lung  and  bronchi  are  dilated  and  tortuous.  On  microscopic  exami- 
nation, the  pulmonary  capillaries  may  be  found  dilated  to  several 
times  their  normal  width  and  the  interstitial  tissue  is  increased  in 
amount.  Pigment  granules  may  be  present  in  the  interstitial  tissue 
and  within  the  alveolar  cells.  Pigmented  epithelial  cells  ("Herz- 
fehlerzellen")  may  also  be  found  in  the  sputum. 

Pulmonary  stasis  from  cardiac  insufficiency  causes  dyspnea,  cyanosis, 


320  DISEASES  OF   THE  LUNGS 

and  cough.  These  symptoms  are  likely  to  be  intensified  in  those 
eases  of  cardiac  insufficiency  in  which  the  force  of  the  left  ventricle 
suffers  relatively  greater  impairment  than  the  right.  They  are  likely 
to  make  their  appearance  early  in  the  course  of  mitral  stenosis  in 
which  the  outflow  from  the  lungs  is  not  only  obstructed,  but  the 
stasis  is  increased  by  the  hypertrophied  right  ventricle.  Likewise 
in  other  conditions  of  cardiac  failure  in  which,  with  insufficiency  of 
the  left  ventricle,  the  right  ventricle  still  continues  to  force  blood 
strongly  into  the  lungs,  the  pulmonary  symptoms  are  likely  to  be 
pronounced.  When,  however,  the  right  ventricle  gives  way,  the 
venous  stasis  is  distributed  back  through  the  systemic  veins  and  the 
pulmonary  symptoms  are  likely  to  be  less  marked. 

The  dyspnea  of  passive  pulmonary  congestion  has  been  ascribed  to 
various  factors.  It  has  led  to  much  discussion  and  difference  of  opinion, 
and  a  satisfactory  explanation  cannot  yet  be  offered.  Obstruction 
of  the  outflow  of  blood  from  the  lungs  to  the  heart  leads  to  over- 
filling of  the  pulmonary  capillaries,  slowing  of  the  pulmonary  blood 
stream,  and  distention  and  diminished  elasticity  of  the  lung.  The 
mechanical  changes  in  the  lung  limit  the  amplitude  of  pulmonary 
excursion,  overburden  the  respiratory  muscular  system,  and  dyspnea 
results.  Inasmuch  as  the  freedom  with  wdiich  the  lungs  can  expand 
is  limited  by  the  structures  which  surround  them,  the  pulmonary 
alveoli  are  probably  narrowed,  as  maintained  by  Traube,  and  the 
respiratory  surface  thus  diminished  in  extent.  A  diminished  amount 
or  impairment  in  the  quality  of  the  blood  supply  to  the  respiratory 
centre  may  be  regarded  as  contributing  factors. 

A  striking  feature  of  cardiac  dyspnea  is  the  frequency  with  which 
it  is  intensified  in  the  reclining  position.  Ability  to  breathe  more 
easily  in  the  upright  position  (orthopnea)  may  be  due  to  increased 
thoracic  space  from  the  descent  of  the  liver  and  the  diaphragm, 
diminished  venous  stasis  in  the  medulla  and  relief  of  the  pulmonary 
congestion  from  slowing  of  the  venous  circulation  in  the  territory 
drained  by  the  inferior  vena  cava,  in  the  sitting  position. 

Cough  is  a  frequent  symptom.  Expectoration  may  be  absent.  When 
present  in  uncomplicated  cases,  the  sputum  is  usually  scanty  and 
mucoid.  Blood  is  frequently  present,  as  bloody  streaks,  small  bloody 
masses  or  a  frothy  bloody  mucus.  In  rare  instances,  small  blood  clots 
are  expectorated.  Frank  hemorrhage  of  small  amounts  of  blood  may 
occur,  probably  from  the  rupture  of  dilated  vessels  in  the  walls  of  the 
bronchi.  Bronchitis  is  not  infrequently  engrafted  on  the  pulmonary 
congestion  and  then  aggravates  the  pulmonary  symptoms. 

Uncomplicated  passive  congestion  gives  rise  to  no  physical  signs. 
When  associated  with  the  extravasation  of  fluid  into  the  air  passages, 
rales  may  be  heard.  Fever  is  absent.  If  the  stasis  reaches  the  systemic 
venous  circuit,  swelling  of  the  liver  and  edema  of  the  feet  may  com- 
plicate the  situation. 

The  symptoms  of  passive  pulmonary  congestion  are  subject  to 


CIRCULATORY  DISTURBANCES  '/>2\ 

remissions  and  exacerbations  which  depend  on  the  establishment  or 
failure  of  cardiac  compensation. 

Cardiac  Asthma. — Rapid  loss  of  power  in  the  left  ventricle  may  be 
quickly  followed  by  severe  thoracic  oppression,  intense  dyspnea, 
orthopnea,  cyanosis  and  cough  with  scanty,  mucoid,  blood-tinged 
sputum.  The  lungs  may  be  negative  with  the  exception  of  fine, 
non-consonating  rales  at  the  bases.  The  term  "cardiac  asthma" 
has  been  applied  to  this  condition. 

Hypostatic  Congestion. — In  long-standing  passive  congestion,  the 
effect  of  gravity  may  largely  determine  the  location  of  the  process, 
which  is  then  most  marked  in  the  dependent  parts,  as  at  the  bases 
posteriorly  with  the  patient  lying  in  bed.  The  term  "hypostatic 
congestion"  is  applied  to  this  condition. 

Hypostatic  Pneumonia. — Bacterial  invasion  may  be  superimposed 
on  hypostatic  congestion  and  lead  to  "hypostatic  pneumonia." 
The  pneumonia  may  be  lobar,  but  is  more  commonly  lobular.  Owing 
to  the  debilitated  condition  of  the  patient  and  the  coexistence  of 
edema  in  the  affected  region,  the  symptoms  and  physical  signs  are 
likely  to  be  atypical.  Fever  may  or  may  not  be  present.  Existing 
dyspnea  and  cyanosis  may  be  aggravated.  Signs  of  pulmonary  con- 
solidation, consonating  rales,  bronchial  breathing,  increase  of  voice, 
whisper  and  tactile  fremitus  may  be  present  if  the  pulmonary  process 
is  sufficiently  extensive  and  reaches  the  periphery  of  the  lung.  An 
intense  edema,  however,  may  mask  the  signs.  The  complication  adds 
gravity  to  an  already  grave  situation  and  is  not  infrequently  first 
discovered  at  postmortem  examination. 

Diagnosis. — Passive  hyperemia  of  the  lung  may  be  suspected  in 
the  presence  of  cardiac  insufficiency  involving  the  left  ventricle  and 
in  uncompensated  mitral  stenosis.  Some  confirmation  of  its  presence 
is  afforded  by  the  expectoration  of  mucoid  sputum  mixed  with  blood, 
if  pulmonary  infarction  and  pneumonia  can  be  excluded. 

Prognosis. — Passive  congestion  of  the  lung  is  responsible  for  the 
earliest  symptoms,  indicating  cardiac  decompensation.  The  outlook 
is  that  of  the  disease  to  which  the  passive  congestion  is  secondary. 
Hypostatic  pneumonia  is  an  unfavorable  complication  and  is  likely 
to  hasten  a  fatal  termination. 

Treatment. — Treatment  should  be  directed  to  the  cardiac  affection 
upon  which  the  passive  congestion  depends.  With  hypostatic  pneu- 
monia, an  expectorant  such  as  ammonium  chloride  may  be  tried. 

Pulmonary  Edema. — In  this  condition  there  is  an  escape  of  fluid 
from  the  pulmonary  vessels  into  the  pulmonary  tissue,  the  alveoli, 
the  bronchioles,  and  frequently  into  the  bronchi  also.  It  is  a  very 
common  postmortem  finding  and  often  precedes  death  by  only  a  short 
interval.  It  is  then  spoken  of  as  a  terminal  or  final  edema.  It  may 
also  occur  as  a  transient  condition  in  the  course  of  mild  or  severe 
pulmonary  or  other  lesions.  Its  gravity  varies  much  with  the  extent 
of  the  process,  the  cause  and  the  rapidity  with  which  it  occurs.  In 
21 


■Y22  DISEASES  OF  THE  LUNGS 

general,  it  may  be  said  that  pulmonary  edema  is  a  relatively  unim- 
portant event,  patients  dying  with  rather  than  of  it.  In  some 
instances  it  is  a  contributing  or  principal  cause. 

Chronic  Form. — As  already  noted,  long-standing,  passive  conges- 
tion of  the  lung  is  likely  to  be  most  marked  at  the  bases.  Such 
hypostatic  congestion  is  likely  soon  to  be  followed  by  the  escape  of 
fluid  from  the  vessels  in  the  affected  region.  The  condition  is  then 
spoken  of  as  "hypostatic  edema,"  which  varies  in  degree  from  a  slight 
excess  of  moisture  to  an  airless  and  solid  lung.  Hypostatic  conges- 
tion and  edema  are  bilateral  or  unilateral,  depending  on  the  prevailing 
position  of  the  patient  on  the  back  or  on  one  or  the  other  side.  A 
half  or  more  of  one  or  both  lungs  may  thus  be  affected.  Rales  may 
be  heard  over  the  site  of  the  process.  If  the  edema  is  marked,  there 
is  dulness,  diminished  or  absent  breathing,  voice,  whisper  and  tactile 
fremitus.  It  may  be  difficult  or  impossible  to  differentiate  this  con- 
dition from  hydrothorax  without  exploratory  puncture.  Pleural 
effusion,  however,  may  complicate  the  edema! 

The  treatment  of  hypostatic  edema  is  that  of  the  cardiac  affection 
upon  which  the  edema  depends.  When  the  patient  is  confined  to  the 
bed,  an  effort  should  be  made  to  avoid  the  development  of  hypostatic 
congestion  and  edema  by  frequently  changing  the  position  from  one 
side  to  the  other  and  the  back.  If  his  strength  permits  the  patient 
may  also  be  propped  up  with  pillows  or  a  bed  rest. 

Acute  Form. — This  is  associated  with  a  variety  of  pathologic 
conditions. 

1.  Cardiac  Disease. — Cardiac  weakness,  whether  from  diseases  of 
the  heart  itself  or  secondary  to  arteriosclerosis  or  renal  disease,  must 
be  regarded  as  one  of  the  chief  causes  of  pulmonary  edema. 

2.  Renal  Lesions. — Chronic  Bright's  disease  and  arteriosclerosis 
are  common  findings  in  cases  of  pulmonary  edema.  The  nephritis 
is  commonly  only  indirectly  a  cause,  through  its  effect  on  the  heart 
and  aorta.  It  is  possible,  however,  that  both  edema  of  the  lungs 
and  edema  of  the  glottis  may  be  due  to  toxemia. 

3.  Arteriosclerosis. — This  is  frequently  present.  The  arteriosclerosis 
may  affect'the  aorta  alone  or  may  be  general.  Huchard1  regards  the 
pulmonary  edema  as  due  to  extension  of  the  aortitis  and  periaortitis 
to  the  cardiopulmonary  plexus  with  consequent  disturbance  of 
innervation  in  the  pulmonary  vessels.  It  seems  more  probable,  how- 
ever, that  here  also  the  arteriosclerosis  is  responsible  for  the  edema 
through  its  effect  on  the  heart. 

4.  Infectious  Disease. — Acute  pulmonary  edema  may  be  observed 
in  the  course  of  typhoid  fever,  tuberculosis,  rheumatic  fever,  scarlet 
fever,  smallpox,  influenza,  and  pneumonia.  Cardiovascular  or  renal 
disease  is  frequently  present  and  diminished  resistance  to  infection 
from  passive  congestion  may  be  in  part  responsible.    In  some  instances 

1  Bull,  de  l'Acad.  de  Med.,  1897,  xxxvii,  509;  and  Bull,  med.,  1897,  xi,  400. 


CIRCULATORY  DISTURBANCES  323 

the  edema  is  the  initial  stage  of  an  inflammatory  process  which  has 
progressed  beyond  a  simple  active  hyperemia,  and  yet  is  not  out- 
spoken enough  to  be  classed  as  pneumonia.  The  pneumococcus  is 
most  frequently  found  in  the  affected  regions.  Streptococci  and 
other  organisms  are  also  found. 

5.  Paracentesis  of  the  Thorax  and  Abdomen. — In  rare  instances, 
acute  pulmonary  edema  and  the  expectoration  of  albuminous  fluid 
follow  the  removal  of  pleural  effusion.  The  cause  of  the  edema 
cannot  be  stated.  It  is  improbable  that  it  is  due  to  injury  of  the  lung 
by  the  trocar.  The  albuminous  expectoration  may  follow  the  with- 
drawal of  small  amounts  of  fluid,  but  in  general,  it  has  occurred  after 
the  removal  of  large  quantities.  The  postmortem  reports  on  the 
fatal  cases  suggests  that  pulmonary  inelasticity  from  pleural  adhesions 
or  complicating  cardiac,  pulmonary  or  mediastinal  disease  is  an 
important  contributing  factor.  The  condition  may  be  due  to  con- 
gestion of  the  expanding  lung,  and  the  ready  escape  of  serum  from 
vessels  rendered  more  permeable  by  reason  of  long  compression. 
Riesman1  has  termed  this  "congestion  by  recoil."  It  is  also  possible 
that  the  condition  is  an  "edema  ex  vacuo,"  undue  negative  tension 
in  the  aspirator  serving  to  forcibly  expand  an  inelastic  lung  and  thus 
withdraw  fluid  from  the  vessels.  Pulmonary  edema  has  also  followed 
withdrawal  of  abdominal  fluid. 

6.  Doubtful  Causes. — Isolated  examples  have  been  reported  of 
pulmonary  edema  during  pregnancy,  in  the  course  of  tabes  dorsalis, 
in  hysteria,  as  a  manifestation  of  angioneurotic  edema  and  after 
anesthesia.  Such  cases  probably  belong  among  the  groups  previously 
mentioned. 

Pathogenesis. — The  pulmonary  edema  accompanying  infections  and 
following  paracentesis  need  not  be  further  considered. 

Concerning  the  edema  arising  in  the  course  of  cardiorenal  or 
cardiovascular  disease,  it  may  be  assumed  that  it  is  due  to  increased 
pressure  within  the  pulmonary  capillaries  or  an  increase  in  their 
permeability  singly  or  combined. 

It  is  probable  that  the  escape  of  fluid  from  the  vessels  is  for  the 
most  part  mechanical  and  cardiac  in  origin.  Myocardial  weakness 
is  commonly  present,  but  weakness  of  the  heart  as  a  whole,  frequently 
fails  to  cause  pulmonary  edema  and  is  thus  not  a  sufficient  explanation. 
Welch's2  experimental  production  of  pulmonary  edema  in  rabbits 
by  squeezing  the  left  ventricle  seems  to  offer  the  true  explanation. 
Partial  paralysis  of  the  left  ventricle  resulted  from  the  mechanical 
irritation  while  the  right  ventricle  still  continued  to  beat.  Incapacity 
of  the  left  ventricle  to  expel  the  blood  onward  diminishes  the  outflow 
from  the  lungs.  Persistent  action  of  the  right  ventricle  overfills  the 
pulmonary  circuit,  and  serum  escapes  from  the  distended  capillaries. 

1  Amer.  Jour.  Med.  Sci.,  April,  1902. 

2  Virchow's  Arch.,  1878,  vol.  lxxii;  and  also  Meltzer,  Amer.  Med.,  1904,  viii,  19,  59, 
151,  and  191. 


324  DISEASES  OF  THE  LUNGS 

Acute  pulmonary  edema,  according  to  Welch,  is  thus  due  to  "a  dis- 
proportion between  the  working  power  of  the  left  ventricle  and  the 
right  ventricle  of  such  a  character  that,  the  resistance  remaining 
the  same,  the  left  ventricle  is  unable  to  expel  in  a  unit  of  time  the 
same  quantity  of  blood  as  the  right  ventricle." 

Arterial  hypertension  may  be  suspected  to  underly  the  condition. 
The  left  ventricle,  already  taxed  nearly  to  its  limit,  is  still  further 
burdened,  it  may  be  by  undue  physical  effort  or  excitement,  and 
suddenly  gives  way  under  the  strain.  Further  observations  on  the 
behavior  of  the  blood  pressure  in  such  cases  are  needed.  A  disturb- 
ance in  the  coronary  artery  leading  to  insufficiency  of  the  left  ventricle 
is  also  a  possible  explanation.  Kraus1  finds  that  an  intense  pulmonary 
edema  may  be  obtained  in  rabbits  injected  intravenously  with  200 
to  300  c.c.  of  normal  salt  solution  if  both  vagi  are  cut  in  the  neck 
following  the  injection.  He  ascribes  the  edema  to  loss  of  vasomotor 
tone  in  the  pulmonary  vessels. 

While  inequality  in  the  capacity  of  the  two  ventricles  from  what- 
ever source  seems  the  most  important  factor  in  acute  pulmonary 
edema,  yet  an  increased  vascular  permeability  cannot  be  excluded  as 
a  contributing  cause. 

Pathology. — The  appearance  of  the  lungs  depends  upon  the  associa- 
tion of  the  edema  with  active  or  passive  hyperemia.  The  essential 
addition  to  these  conditions  is  the  presence  in  the  alveoli,  the  bron- 
chioles and  the  bronchi  also,  of  an  abnormal  amount  of  serous  fluid, 
which  exudes  from  the  cut  surface  of  the  lung.  The  fluid  may  be 
foamy  from  admixture  with  air.  Pulmonary  edema  arising  in  conse- 
quence of  inflammatory  processes  is  usually  limited  to  the  neighbor- 
hood of  such  conditions,  and  may  thus  be  local  and  circumscribed, 
or  general  in  a  part  or  the  whole  of  one  or  more  lobes  of  the  lungs. 
Depending  on  the  intensity  of  the  inflammatory  process,  the  fluid 
is  more  or  less  tinged  with  blood.  It  is  rich  in  albumin  and  is  found 
on  microscopic  examination  to  contain  desquamated  alveolar  epithe- 
lium, red  blood  corpuscles,  varying  numbers  of  poly  nuclear  leukocytes 
and  bacteria.  When  the  edema  is  due  to  stasis,  it  is  bilateral.  It  may 
be  confined  to  the  lower  lobes  or  involve  the  whole  of  both  lungs,  in 
which  case  it  is  most  marked  at  the  bases.  The  fluid  may  be  blood 
tinged.  Desquamated  alveolar  epithelial  cells  are  present  in  varying 
and  usually  small  numbers. 

Symptoms. — Pulmonary  edema  is  usually  only  a  relatively  unim- 
portant event  in  the  course  of  active  hyperemia  or  of  stasis,  and  is 
commonly  indicated  only  by  an  aggravation  of  already  existing 
dyspnea  and  cough,  with  the  presence  of  rales  over  the  involved  region. 
At  times,  the  sudden  occurrence  of  an  intense  and  widespread  edema 
may  prove  rapidly  fatal.  In  such  cases  the  patient  may  die  of  suffoca- 
tion, and  before  he  has  had  time  or  strength  to  expectorate  the  fluid. 

1  Berl.  klin.  Woch.,  1913,  i,  1035. 


CIRCULATORY  DISTURBANCES  325 

Pulmonary  edema  due  to  an  acute  infection  of  the  lung  is  seldom  sudden 
in  onset,  is  accompanied  by  fever,  and  the  expectoration  is  usually 
only  moderate  in  amount. 

In  some  instances  the  expectoration  of  a  large  amount  of  serous 
fluid  is  a  prominent  feature.  These  cases  are  usually  associated 
with  cardiovascular  or  renal  disease  or  both.  The  onset  is  usually 
sudden.  The  attack  is  likely  to  occur  at  night  or  after  unusual  exertion 
or  excitement.  It  may  wake  the  patient  from  sleep.  There  is  a  sense 
of  severe  thoracic  oppression  which  increases  rapidly  to  a  feeling  of 
impending  suffocation.  The  breathing  is  labored  and  accompanied 
by  audible  rattling  noises.  Speech  is  difficult  or  impossible.  The 
dyspnea  becomes  intense.  Orthopnea  is  present.  The  face  and 
extremities  become  cold  and  cyanotic  and  the  skin  may  be  bathed 
in  sweat.  A  constant  and  harassing  cough  accompanies  the  paroxysm. 
The  expectoration  is  pale  or  slightly  reddish,  thin  watery  fluid,  inti- 
mately mixed  with  air,  which  gives  it  a  foamy  appearance.  It  may 
at  times  actually  gush  from  the  mouth  and  amount  to  as  much  as  one 
to  two  quarts  during  the  attack.  The  paroxysm  usually  lasts  for 
several  hours.  The  patient  may  die  in  the  first  attack.  More  often 
he  recovers,  but  recurrences  are  common.  Lissamen's1  patient,  a 
woman,  aged  forty-five  years,  had  seventy-two  attacks,  all  nocturnal, 
within  two  and  a  half  years. 

Examination  during  the  attack  shows  coarse  bubbling  rales  through- 
out the  lungs,  usually  most  marked  at  the  bases,  where  there  may 
also  be  slight  dulness.  The  cardiac  sounds  may  be  obscured  or 
inaudible  in  consequence  of  the  rales.  In  some  instances,  weakness 
of  the  cardiac  impulse  and  feeble  pulse  have  been  noted.  Fever  is 
absent  in  uncomplicated  cases.  Manifestations  of  dropsy  elsewhere 
than  in  the  lungs  may  or  may  not  be  present.  In  all  but  one  of 
Stengel's2  five  cases  the  blood  pressure  was  high.  Aphasia,  mono- 
plegia, hemiplegia,  delirium,  stupor,  coma  or  convulsions  may  be 
observed  during  the  attack. 

Diagnosis. — Attacks  of  so-called  cardiac  or  uremic  asthma,  like 
attacks  of  pulmonary  edema,  are  probably  due  to  cardiac  weakness, 
and  especially  to  failure  of  the  left  ventricle.  The  difference  between 
them  and  pulmonary  edema  may  be  regarded  largely  as  one  of  degree 
in  the  disproportion  between  the  working  power  of  the  two  ventricles. 
The  acute  passive  congestion  of  cardiac  asthma  is  unaccompanied 
by  the  outpouring  of  an  abundant  serous  fluid  as  in  pulmonary  edema. 

Acute  pulmonary  edema  should  be  distinguished  from  bronchial 
asthma  in  which,  however,  the  dyspnea,  while  affecting  both  phases 
of  respiration,  is  especially  expiratory.  The  expectoration  is  scanty 
and  mucoid,  rather  than  abundant  and  watery.  The  thorax  is  dis- 
tended.   Sibilant  and  sonorous  rales  are  heard  on  auscultation.    Cursch- 

1  Lancet,  February  8,  1902. 

2  Paroxysmal  Pulmonary  Edema  and  its  Treatment,  Amer.  Jour.  Med.  Sci.,  January, 
1911. 


32G  DISEASES  OF  THE  LUNGS 

niann  spirals  and  Charcot-Leyden  crystals  in  the  sputum  and  an 
increase  of  eosinophils  in  the  sputum  and  the  Mood  may  be  helpful 
features.  The  presence  of  cardiorenal  or  cardiovascular  disease, 
with  arterial  hypertension,  may  be  established  in  pulmonary  edema. 

Prognosis. — This  is  grave.  The  patient  may  die  in  the  first  attack. 
More  commonly  he  recovers,  but  recurrences  are  frequent  at  long 
or  short  intervals,  between  which  there  is  likely  to  be  a  progressive 
failure  of  cardiac  compensation. 

Treatment. — The  pulmonary  edema  arising  in  the  course  of  infections 
of  the  lung  is  to  be  treated  as  for  the  underlying  condition. 

The  treatment  of  acute  pulmonary  edema  which  occurs  in  conse- 
quence of  cardiorenal  or  cardiovascular  disease  presents  a  difficult 
problem.  In  the  present  state  of  our  knowledge  the  attacks  may  be 
regarded  as  due  to  cardiac  insufficiency  of  such  a  character  that  the 
relative  power  of  the  two  sides  of  the  heart  is  disturbed,  the  essential 
feature  being  a  loss  of  strength  in  the  left  ventricle.  Arterial  hyper- 
tension or  disease  of  the  coronary  arteries,  or  both,  may  underly 
the  condition.  The  indication  is  to  reestablish  cardiac  efficiency  as 
a  whole  and  to  equalize  the  work  of  the  right  and  left  ventricles.  The 
situation  is  complicated,  is  not  well  understood,  and  the  treatment 
so  far  as  the  giving  of  drugs  is  concerned,  is  largely  empirical. 

Complete  mental  and  physical  rest  is  of  chief  importance,  and  should 
as  far  as  possible  be  secured.  The  patient  should  be  abed.  He  is 
usually  more  comfortable  propped  up  with  pillows  or  a  bed-rest. 
Morphin  has  been  strongly  recommended  and  as  strongly  condemned. 
It  is  chiefly  of  value  through  its  quieting  effect  on  the  nervous  system. 
Though  it  is  said  by  some  to  increase  the  danger  of  suffocation,  this 
is  probably  overestimated,  and  it  may  be  used  with  advantage  in  cases 
in  which  there  is  much  nervous  excitement,  in  doses  of  grs.  I  or  \ 
(0.008  or  0.016  gm.)  subcutaneously.  Oxygen  inhalations  are  harmless 
and  may  do  good.  Counter-irritation  to  the  skin  may  be  followed  by 
improvement.  A  half  dozen  or  more  dry  cups  may  be  applied  to  the 
back  and  an  equal  number  to  the  front  of  the  chest.  A  mustard  poul- 
tice or  plaster  may  be  applied  to  the  front  of  the  chest  and  allowed 
to  remain  until  the  skin  is  well  reddened,  but  not  longer.  Hot  hand 
and  foot  baths  with  or  without  the  addition  of  mustard  may  also  be 
used. 

The  attempt  to  stimulate  the  heart  by  means  of  drugs  should  be 
made  only  after  careful  consideration  of  the  circulatory  condition. 
It  is  quite  possible  to  do  more  harm  than  good.  It  seems  best  to  rely 
on  the  simple  measures  already  suggested  unless  for  special  reasons 
it  seems  wise  to  do  more.  In  considering  the  advisability  of  cardiac 
stimulation,  the  probable  disproportion  in  the  action  of  the  two  ven- 
tricles must  be  borne  in  mind.  It  is  important  to  know  whether  the 
failure  of  the  left  ventricle  is  due  to  arterial  hypertension  or  to  some 
other  cause.  If  arterial  hypertension  has  been  the  cause,  strophanthin, 
given  intravenously,  combined  with  the  use  of  nitroglycerine  or  amyl 


CIRCULATORY  DISTURBANCES  327 

nitrite    may    be   of   service.     When    other    measures    fail    digitalis, 
camphor,  and  caffein,  may  be  used. 

Emerson1  recommends  artificial  respiration  for  pulmonary  edema 
due  to  cardiac  insufficiency,  believing  that  the  flow  of  blood  through 
the  lungs  will  thereby  be  promoted  and  the  right  heart  relieved.  In 
desperate  cases,  with  deep  cyanosis  and  increase  in  the  cardiac  dulness 
to  the  right,  venesection  may  be  done. 

1  Arch.  Int.  Med.,  1909,  iii,  368. 


CHAPTER  XVIII. 
PULMONARY  THROMBOSIS,  EMBOLISM  AND  INFARCTION. 

Thrombosis. — By  pulmonary  thrombosis  is  understood  the  forma- 
tion during  life  from  the  constituents  of  the  blood  of  a  solid  mass  or 
plug  within  the  pulmonary  vessels.  Such  plugs  or  thrombi  may  be 
formed  in  the  pulmonary  veins,  the  pulmonary  arteries  or  their 
branches.  Thrombosis  of  the  pulmonary  veins  may  give  rise  to 
emboli  in  the  systemic  arterial  circulation. 

Embolism. — Pulmonary  embolism  may  arise  in  consequence  of  the 
detachment  of  a  part  or  the  whole  of  a  thrombus  from  the  pulmonary 
artery,  the  systemic  veins  or  the  right  side  of  the  heart. 

The  two  processes  may  well  be  considered  together. 

Occurrence. — Pulmonary  thrombosis  and  embolism  are  of  infre- 
quent occurrence.  Among  3000  autopsies  at  the  Massachusetts 
General  Hospital,  pulmonary  thrombosis  or  embolism  is  recorded  in 
only  60  instances.  The  condition  is  somewhat  more  frequent  than 
these  figures  indicate,  since  cases  may  be  unrecognized  during  life  and 
followed  by  recovery. 

Etiology. — The  factors  which  lead  to  thrombosis  in  any  part  of  the 
body  apply  also  to  its  occurrence  in  the  pulmonary  vessels.  Certain 
alterations  in  the  blood  itself  undoubtedly  play  an  important  part  in 
the  predisposition  to  thrombus  formation,  but  as  yet  are  little  under- 
stood. Mechanical  interference  with  the  circulation  is  an  important 
predisposing  cause.  Lesions  of  the  walls  of  the  vessels  also  play  an 
important  part.  Such  lesions  may  be  bacterial,  toxic  or  mechanical 
in  origin.  The  various  factors  are  often  combined.  Similar  causes 
influence  the  occurrence  of  pulmonary  embolism,  as  a  secondary  mani- 
festation, but  all  thrombi  are  not  equally  likely  to  give  rise  to  emboli. 

In  the  majority  of  cases  in  which  plugs  are  found  in  the  pulmonary 
arteries  or  their  branches,  venous  thrombi  are  present  also  in  other 
parts  of  the  venous  circuit.  Thus  of  the  60  cases  in  this  series, 
thrombosis  of  other  venous  channels  was  found  in  36,  including  9 
instances  in  which  2,  4,  and  3  other  channels  were  involved.  In 
cases  with  multiple  plugging  of  vessels,  the  different  veins  affected 
are  usually  those  in  the  line  of  the  blood  current  from  the  involved 
region.  Unrelated  tributaries  in  the  venous  circuit  were  plugged  in 
only  one  instance  in  the  series.  It  is  probable,  therefore,  that  in  the 
majority  of  cases,  plugging  of  the  pulmonary  arteries  or  their  branches 
is  due  to  embolism  rather  than  to  thrombosis,  although  it  is  often 
difficult  to  make  the  distinction  from  the  character  of  the  plug  found 
in  the  pulmonary  vessel. 


THROMBOSIS,  EMBOLISM  AND  INFARCTION  329 

Thrombosis  of  the  veins  of  the  lower  extremities  is  the  most  common 
source  of  pulmonary  embolism.  Thrombosis  of  the  right  side  of  the 
heart,  the  iliac,  uterine  and  ovarian  veins  and  the  cerebral  sinuses 
are  frequent  sources.  The  hemorrhoidal,  prostatic,  innominate  and 
jugular  veins  and  those  of  the  upper  extremities  are  among  the 
numerous  occasional  sources  of  pulmonary  emboli. 

Of  the  various  diseases  with  which  pulmonary  embolism  is  associated 
those  in  which  venous  thrombosis  is  a  frequent  complication  naturally 
occupy  an  important  place.  In  general,  pulmonary  embolism  arises 
more  frequently  from  septic  than  from  bland  thrombi. 

Cardiac  disease  from  its  effect  on  the  circulation  is  an  important 
predisposing  cause  of  pulmonary  thrombosis  and  embolism.  In  this 
series,  plugging  of  the  pulmonary  arteries  complicated  cardiac  hyper- 
trophy and  dilatation  in  28  instances,  in  five  of  which  thrombi  in  the 
right  auricle  or  ventricle  were  a  possible  source.  In  nine  of  the  cases 
there  was  valvular  endocarditis.  The  places  of  election  for  intra- 
cardiac thrombi  are  the  auricular  appendices  and  the  region  between 
the  columnar  carnese  at  the  apices  of  the  ventricles.  It  is  possible  that 
an  open  foramen  ovale  may  furnish  the  channel  through  which  emboli 
may  pass  from  the  left  to  the  right  auricle  and  finally  lodge  in  the  pul- 
monary artery.  I  know  of  no  instance  in  which  such  an  occurrence 
has  been  reported.  In  one  case  (Autopsy  733)  in  this  series,  two 
openings  in  the  foramen  ovale,  measuring  about  2  and  4  mm.  respec- 
tively, were  occluded  by  thrombi  which  passed  through  the  openings. 
These  plugs  projected  at  either  side  into  the  right  and  left  auricles 
and  united  to  form  one  continuous  thrombus.  The  right  auricle  and 
ventricle  also  contained  thrombi,  while  the  left  side  of  the  heart  was 
free. 

Pulmonary  thrombosis  or  embolism  is  not  very  infrequent  as  a 
terminal  event  in  many  cachectic  conditions.  Venous  stasis  and 
terminal  infections  undoubtedly  play  an  important  part  in  their  pro- 
duction. They  are  of  little  clinical  interest  and  need  not  be  considered 
in  detail.  Malignant  disease  occupies  a  prominent  place  and  is  repre- 
sented by  ten  instances  in  this  series. 

Venous  thrombosis  complicating  the  puerperium  is  not  uncommonly 
a  cause  of  pulmonary  embolism.  The  venous  thrombosis  may  occur 
during  pregnancy,  but  is  much  more  frequent  within  the  first  few  days 
after  delivery.  The  veins  of  the  lower  extremity  are  apparently 
prevailingly  involved.  In  many  instances,  the  process  has  arisen  by 
extension  from  the  pelvic  veins,  the  invasion  of  which  may  in  turn 
come  from  the  uterine  sinuses.1  Herff2  estimates  the  occurrence  of 
venous  thrombosis  at  about  2  per  cent,  of  all  lying-in  women.  Pul- 
monary embolism  occurs  in  from  15  to  20  per  cent,  of  those  with 
venous  thrombosis.    The  mortality  is  estimated  at  about  50  per  cent. 

1  Sperling,  Zur  Kasuistik  der  Embolie  der  Lungenarterie,  etc.,  Zeit.  f.  Geburtshulfe 
und  Gynakologie,  1893,  vol.  xxvii. 

2  Handbuch  der  Geburtshulfe,  III,  ii,  974. 


330  DISEASES  OF  THE  LUNGS 

In  a  small  proportion  of  cases,  pulmonary  embolism  may  occur  without 
previous  symptoms  of  venous  thrombosis.  Such  emboli  probably 
come  from  thrombi  in  the'  pelvic  veins. 

Thrombosis  occurring  in  typhoid  fever  may  give  rise  to  pulmonary 
embolism,  as  in  four  cases  in  this  scries.  Thayer1  mentions  only  one 
case  of  pulmonary  plugging  in  38  instances  of  venous  thrombosis 
among  1458  cases  of  typhoid  fever. 

Thrombosis  of  the  pulmonary  artery  complicated  pneumonia  in 
only  one  case.  This  was  the  only  thrombus  found.  The  incidence 
of  this  complication  may  be  estimated  from  the  statistics  of  Musser 
and  Norris.2  They  found  peripheral  thrombosis  in  17  (0.7-2  per  cent.) 
of  2360  and  pulmonary  thrombosis  in  5  (0.27  per  cent.)  of  1830  col- 
lected cases  of  pneumonia.  Steiner3  reported  on  41  cases  of  peripheral 
thrombosis  complicating  pneumonia,  finding  it  more  common  during 
convalescence.  Death  was  due  to  pulmonary  embolism  in  5  cases. 
Thrombosis  of  the  pulmonary  veins  is  a  constant  feature  of  pneumonia 
and  may  give  rise  to  emboli  in  the  systemic  arterial  circuit. 

Pulmonary  tuberculosis  is  complicated  by  venous  thrombosis  in 
rare  instances.  Dodwell4  observed  it  in  20  of  1300;  Ruge  and  Hierokles5 
in  19  of  1778  cases.  It  usually  occurs  in  the  last  few  weeks  or  months 
of  life,  and  is  probably  due  to  cardiac  weakness  and  terminal  infection 
in  most  instances.  The  thrombus  is  commonly  in  the  peripheral 
veins,  but  the  pulmonary  artery  wras  involved  in  two  of  Ruge  and 
Hierokles'  series. 

In  pleurisy  with  effusion,  thrombosis  or  embolism  is  one  of  the 
most  frequent  causes  of  sudden  death.  In  a  series  of  500  cases  with 
serofibrinous  effusion,  sudden  death  before  tapping  occurred  in  3, 
and  autopsy  showed  the  cause  of  death  in  2  to  be  pulmonary 
embolism.  One  patient  had  a  double  effusion,  the  second  a  large  unila- 
teral accumulation.  Of  14  cases  with  pleurisy  with  effusion  coming 
to  autopsy,  thrombosis  or  embolism  of  the  pulmonary  artery  was  a 
cause  of  sudden  death  in  5.  Of  the  5  cases,  3  had  pleurisy  with 
serofibrinous,  2  with  purulent  effusion.  Bacterial  infection  may  play 
a  part  in  causing  this  complication.  Venous  stasis  from  the  pleural 
fluid  is  probably  also  an  important  factor.  The  most  common  sources 
of  emboli  in  patients  with  pleural  effusion  are  from  thrombi  within 
venous  channels  not  far  distant  from  the  lung,  as  the  pulmonary 
arteries,  the  right  auricle,  the  superior  and  inferior  vena  cava,  the  iliac 
and  femoral  veins.  The  large  size  of  the  vessels  involved  increases  the 
danger  of  a  fatal  termination  from  the  large  size  of  the  detached 
embolus.  If  life  is  prolonged,  pulmonary  infarction  is  favored  by  the 
existing  pulmonary  stasis. 

1  Johns  Hopkins  Hosp.  Bull.,  October,  1904. 

2  Osier's  Mod.  Med.,  vol.  ii,  p.  611. 

3  Johns  Hopkins  Hosp.  Bull.,  June,  1902. 

4  Amer.  Jour.  Med.  Sci.,  June,  1893. 
s  Berl.  klin.  Woch.,  1899,  No.  4. 


THROMBOSIS,  EMBOLISM  AND  INFARCTION  331 

Chlorosis  may  be  complicated  by  thrombosis  and  pulmonary 
embolism.  According  to  Eichhorst  (quoted  from  Leichtenstern), 
venous  thrombosis  was  present  in  4  (1.6  per  cent.)  of  243  cases.  Yon 
Noorden1  observed  it  in  5  (2  per  cent.)  of  230  and  Leichtenstern2  in 
11  (0.66  per  cent.)  of  1653  cases.  Involvement  of  the  lower  extremities 
(48  cases)  and  the  cerebral  sinuses  (29  cases)  comprised  77  of  the  86  cases 
in  Leichtenstern's  table.  He  found  that  of  52  instances  of  chlorotic 
thrombosis  of  the  extremities,  pulmonary  embolism  occurred  in  10, 
ending  fatally  in  9.  Welch3  collected  13  instances  (25  per  cent.)  of 
pulmonary  embolism  among  52  cases  with  venous  thrombosis  in  other 
regions  than  the  venous  sinuses.  All  but  2  ended  fatally.  This  fre- 
quency of  pulmonary  embolism  gives  an  unusual  gravity  to  this  form 
of  thrombosis.  Its  occurrence  has  been  ascribed  to  peculiar  brittleness 
of  the  chlorotic  thrombi. 

Venous  thrombosis,  followed  by  pulmonary  embolism,  may  com- 
plicate various  operative  procedures. 

According  to  Clark,4  venous  thrombosis  was  observed  35  times  in 
3000  abdominal  sections  at  the  Johns  Hopkins  Hospital.  The  throm- 
bosis involved  the  veins  of  the  legs  and  occurred  from  the  eighth  to 
the  thirtieth  day  after  operation,  being  most  frequent  about  the 
fifteenth  day.  In  an  analysis  of  1196  laparotomies  at  the  Munich 
Surgical  Clinic,  Gebele5  found  77  (6.43  per  cent.)  with  pulmonary 
complications.  Fourteen  (1.17  per  cent.)  were  due  to  pulmonary 
embolism.  Eleven  of  these  were  fatal  and  the  diagnosis  was  confirmed 
by  autopsy.  The  complication  may  occur  without  infection  of  the 
wound  of  operation  or  the  peritoneum  as  in  6  of  his  cases. 

Sonnenburg6  reported  50  cases  (5  per  cent.)  of  thrombosis  and 
embolism  among  1000  operations  for  appendicitis.  Haward's  figures 
are  somewhat  lower,  with  venous  thrombosis  34  times  among  3774 
cases  of  appendicitis.  A  little  less  than  one-eighth  of  the  cases  with 
thrombosis  were  followed  by  pulmonary  embolism.  Clark  believes 
that  the  usual  femoral  thrombophlebitis  which  occurs  as  a  sequel 
to  celiotomy  starts  from  a  primary  thrombus  in  the  deep  epigastric 
veins,  slowly  propagated  along  the  vessel  until  it  reaches  the  external 
iliac,  where  it  gives  rise  to  a  retrograde  thrombus  in  the  femoral  veins. 
The  thrombosis  may  be  due  to  trauma  alone,  or  follow  latent  or  obvious 
infection. 

Pulmonary  embolism  may  similarly  follow  gynecologic  operations, 
the  reduction  or  radical  cure  of  hernia,  fractures,  dislocations,  lacera- 
tions, and  trauma.  The  trauma  may  induce  venous  thrombosis  which 
may  remain  latent  for  a  time  and  be  discovered  only  after  pulmonary 
embolism  has  occurred.    The  original  injury  may  be  mild  or  severe. 

1  Berl.  klin.  Woch.,  1899,  No.  4.  2  Munch,  med.  Woch.,  1899,  No.  48. 

3  Allbutt's  System  of  Medicine,  vol.  vi,  p.  202. 

4  Univ.  of  Penna.  Med.  Bull.,  1902-03,  xv,  156. 

6  Beitrage  z.  klinischen  Chiiurgie,  Tubingen,  1904,  vol.  xliii. 

6  Ueber  Lunsenkomplikationen  bei  Appendicitis,  31  Kongr.  d.  Deutsch.  Ges.  f.  Chir., 
1902. 


332  DISEASES  OF  THE  LUNGS 

The  detachment  of  venous  thrombi  with  consequent  pulmonary 
embolism  may  occur  without  obvious  cause,  and  during  sleep.  It 
may  follow  massage,  a  change  from  the  reclining  to  the  sitting  position, 
an  attack  of  cough,  deep  inspiration,  straining  at  stool,  and  especially 
bending  the  affected  limb,  as  at  the  knee  or  hip.  It  is  possible  that 
elevation  of  the  pelvis,  too  long  maintained  in  the  course  of  laparotomies 
for  operation  upon  the  pelvic  organs,  may  induce  cardiac  dilatation  in 
patients  with  weak  hearts,  and  thus  favor  thrombosis  as  suggested 
by  Trendelenburg.1 

Pathology. — 1.  Thrombosis  and  Embolism. — Thrombosis  of  the 
pulmonary  artery  does  not  differ  essentially  from  a  similar  process 
elsewhere.  Displacement  of  a  thrombus  in  the  pulmonary  artery 
or  its  branches  may  give  rise  to  embolism  of  the  same  vessel  or  its 
branches  beyond.  McPhedran  and  Mackenzie2  have  reported  an 
unusual  instance  of  pulmonary  thrombosis.  The  smaller  pulmonary 
vessels  were  the  site  of  an  extensive  endarteritis  and  were  everywhere 
thrombosed.    In  some  places  the  thrombi  were  organized. 

Owing  to  the  large  size  of  the  right  pulmonary  artery,  emboli  more 
frequently  lodge  in  it  than  in  the  left.  The  lower  are  more  frequently 
affected  than  the  upper  lobes.  This  is  probably  due  to  the  larger  size 
of  the  branches  to  these  regions.  Gravity  may  also  favor  this  location. 
Those  factors  which  diminish  the  blood-supply  to  the  right  lung, 
such  as  previous  thrombosis  or  embolism,  contraction  of  the  lung, 
the  pressure  of  pleural  effusion  or  position  may  dispose  to  left-sided 
embolism.  The  size  of  the  embolus  naturally  varies  with  the  caliber 
of  the  vessel  from  which  it  comes,  although  folding  may  increase 
the  diameter  of  an  elongated  mass  and  result  in  the  occlusion  of 
a  larger  vessel.  Elongated  emboli  riding  on  the  bifurcation  of  the 
pulmonary  artery  are  not  uncommon.  Pulmonary  emboli  are  often 
multiple.  The  pulmonary  artery,  the  right  side  of  the  heart  and  the 
venous  tributaries  are  likely  to  be  engorged,  at  times  markedly  dilated 
with  blood. 

Secondary  thrombus  formation  takes  place  about  the  embolus  if 
life  is  prolonged  after  the  accident.  This  may  result  in  the  occlusion 
of  a  previously  incompletely  closed  vessel.  Both  thrombi  and  emboli 
may  be  converted  by  a  process  of  organization  into  solid  or  cavernous 
fibrous  tissue.  In  rare  instances,  a  partial  restoration  of  the  vessel 
lumen  may  take  place. 

2.  Pulmonary  Infarction. — The  gross  appearance  of  pulmonary 
infarcts  was  first  carefully  described  by  Laennec,  who  termed  the 
condition  "  pulmonary  apoplexy."  Although  the  association  of  arterial 
plugging  with  pulmonary  infarction  was  later  noted,  it  was  not  until 
VirchowV  important  researches  on  thrombosis  and  embolism  that 


1  Prakt.  Ergebn.  d.  Geburtshilfe  u.  Gynakologie,  1911,  hi,  68. 

2  Trans.  Assoc.  Amer.  Phys.,  1903. 

3  Virehow,  Ges.  Abhandl.  z.  wissensch.  Med.,  Frankfurt,  a,  M,  1856,  p.  374. 


THROMBOSIS,  EMBOLISM  AND  INF  AUCTION  333 

emboli  were  suspected  as  a  cause.  The  investigations  of  Fanum1 
and  Cohnheim  and  Litten2  showed  that  in  only  a  small  proportion 
of  the  experiments  on  artificial  embolism  did  infarction  of  the  lungs 
occur.  The  manner  of  its  production  has  been  the  subject  of  consid- 
erable discussion.  KuttnerV  and  Litten's4  work  has  thrown  much 
light  on  the  condition. 

(a)  The  Relation  of  Thrombosis  and  Embolism  to  Pulmonary  Infarc- 
tion.— The  pulmonary  arteries  are  terminal  arteries,  as  Cohnheim 
believed,  but  a  free  and  extensive  anastomosis  doubtless  exists  between 
their  finer  branches  through  the  pulmonary  capillaries.  The  bron- 
chial arteries  also  supply  the  pulmonary  tissue.  Their  importance 
in  maintaining  the  blood  supply  to  the  territory  of  the  pulmonary 
artery  is  indicated  by  Kiittner's  experiment.  After  ligation  of  the 
pulmonary  artery  and  the  injection  of  cinnabar  into  the  jugular  vein, 
he  found  this  substance  not  only  in  the  branches  of  the  bronchial 
arteries,  but  also  in  the  pulmonary  capillaries  and  even  in  the  branches 
and  trunk  of  the  ligated  pulmonary  artery.  Under  ordinary  condi- 
tions following  occlusion  of  a  branch  of  the  pulmonary  artery,  the  pul- 
monary circulation  is  probably  sufficiently  maintained  by  the  neigh- 
boring pulmonary  capillaries  and  the  bronchial  arteries  to  prevent 
infarction.  In  the  presence  of  an  impaired  pulmonary  circulation, 
however,  hemorrhagic  infarction  is  likely  to  follow  such  an  occlusion. 
The  source  of  this  hemorrhage  is  difficult  of  explanation.  Cohnheim 
believed  it  to  be  due  to  a  backward  flow  from  the  pulmonary  veins, 
but  Litten's  observations  indicate  that  it  comes  from  the  bronchial 
arteries.  In  his  experiments,  ligation  of  the  pulmonary  artery  and 
veins,  the  bronchial  arteries  remaining  intact,  was  constantly  followed 
by  pulmonary  infarction,  thus  excluding  the  pulmonary  veins  as  a 
necessary  factor.  Ligation  of  the  pulmonary  and  the  bronchial 
artery,  with  its  collaterals  (the  tracheo-esophageal,  pericardiaco- 
phrenic and  pleuromediastinal  arteries),  was  not  followed  by  infarc- 
tion. In  this  experiment,  in  which  the  pulmonary  veins  were  free,  the 
absence  of  infarction  excludes  them  as  a  probable  source. 

In  clinical  cases,  as  in  these  experiments,  an  important  relation 
obtains  between  pulmonary  infarction  and  the  condition  of  the  pul- 
monary circulation.  When  infarction  follows  pulmonary  thrombosis 
or  embolism,  it  is  usually  associated  with  stasis  in  the  pulmonary 
circuit.  Thus  of  60  cases  of  pulmonary  thrombosis  or  embolism,  com- 
ing to  autopsy  at  the  Massachusetts  General  Hospital,  pulmonary 
infarction  was  found  in  28.  In  all  but  one  of  these  28  cases,  there  was 
some  serious  intrathoracic  complication  sufficient  to  cause  embarrass- 
ment of  the  pulmonary  circulation.  In  22  cases,  11  of  which  were 
complicated  by  an  accumulation  of  pleural  fluid,  disease  of  the  endo- 
cardium, myocardium  or  pericardium  was  present.     Two  of  the  28 

1  Virchow's  Archiv,  vol.  xxv,  pp.  308  and  433. 

2  Ibid.,  vol.  lxv,  pp.  99-115.  3  Ibid.,  vol.  Ixxiii,  p.  1878. 
4  Zeit.  f.  klin.  Med.,  Bd.  i,  pp.  131-227. 


334  DISEASES  OF  THE  LUNGS 

cases  were  complicated  by  lobar  pneumonia,  one  by  pulmonary  tuber- 
culosis, and  one  by  pleurisy  with  effusion.  In  one  instance  there  was 
cancer  of  the  stomach  with  extensive  metastases  and  a  large  amount 
of  fluid  in  the  pleural  sacs.  Of  32  cases  with  pulmonary  thrombosis 
or  embolism,  but  without  infarction,  only  17  were  similarly  complicated. 
Usually  under  normal  conditions  and  at  times  even  when  the  pul- 
monary circulation  is  embarrassed,  the  anastomosing  pulmonary 
capillaries  and  the  bronchial  arteries  are  capable  of  maintaining  the 
circulation  in  the  affected  territory.  Other  factors  may  prevent  the 
occurrence  of  infarction.  The  arterial  plugging  may  be  incomplete, 
the  affected  vessel  may  supply  too  small  an  area,  or  death  may  take 
place  too  quickly  after  the  accident. 

It  has  been  thought  that  pulmonary  infarction  could  occur  from 
other  causes  than  pulmonary  embolism  or  thrombosis,  but  this  is 
improbable.  The  arterial  plugging  can  be  demonstrated  in  a  great 
majority  of  the  cases.  This  has  been  regarded  as  a  result  rather  than 
a  cause  of  the  infarction,  but  venous  rather  than  arterial  plugging  is 
likely  to  be  a  consequence  of  infarction.  An  unobstructed  lumen  in  the 
affected  artery  may  intervene  between  the  plug  and  the  area  of  infarc- 
tion. This  is  in  favor  of  its  primary  rather  than  secondary  origin. 
Then,  too,  the  character  of  the  plug  or  the  appearance  of  one  of  its 
extremities  may  definitely  indicate  its  origin  by  fracture  from  a  throm- 
bus in  a  more  remote  vessel.  The  prevailing  situations  for  pulmonary 
infarctions  correspond  to  the  areas  of  distribution  of  the  pulmonary 
vessels  most  commonly  affected  by  thrombosis  or  embolism.  In  their 
sharp  limitation  from  the  surrounding  tissue,  their  situation,  shape, 
consistency  and  microscopic  appearance,  pulmonary  infarcts  resemble 
similar  processes  elsewhere.  Finally,  pulmonary  infarction  may  be 
experimentally  produced  by  artificial  occlusion  of  the  pulmonary 
arteries. 

(b)  Appearance  of  Pulmonary  Infarcts. — Pulmonary  infarcts  are 
almost  invariably  hemorrhagic.1  The  lower  are  more  frequently 
involved  than  the  upper  lobes  and  the  right  side  more  often  than  the 
left.  The  situation  of  pulmonary  infarcts  thus  corresponds  to  that 
of  pulmonary  emboli.  They  are  more  often  multiple  than  single,  are 
usually  peripheral,  and  on  section  conical  or  wedge  shape,  with  the 
apex  of  the  cone  towrard  the  root  of  the  lung,  the  base,  more  or  less 
circular  in  outline,  appearing  beneath  the  pleural  surface.  They  may 
rarely  be  found  entirely  within  the  substance  of  the  lung,  and  are  then 
likely  to  be  more  nearly  spherical.  In  general  they  vary  in  size  from 
a  cherry-stone  to  a  hen's  egg.  Smaller  and  larger  areas  may  be  found, 
and  in  rare  instances  more  than  a  half  of  one  lobe  may  be  involved. 

1  Freyberger  (Trans.  Path.  Soc,  London,  1898,  xliv,  27)  has  reported  a  rare  instance 
of  an  anemic  pulmonary  infarct.  Cardiac  weakness  may  account  for  this  occurrence. 
Welch  (Allbutt's  System  of  Medicine,  1899,  vi,  265)  states  that  in  two  or  three  instances 
he  has  seen  nearly  white  or  pale-red,  fresh  anemic  infarcts  in  densely  consolidated 
lungs. 


THROMBOSIS,  EMBOLISM  AND  INFARCTION  335 

In  recent  cases  the  overlying  pleura  may  be  normal  in  appearance 
but  with  older  infarcts  it  is  likely  to  be  turbid  and  covered  with  a  thin 
layer  of  fibrinous  exudate.  Careful  search  will  usually  disclose  a  plug 
in  an  artery  at  or  near  the  apex  of  the  infarction.  The  cut  surface  of 
recent  infarcts  is  elevated,  smooth  or  slightly  granular,  dark  red  or 
even  almost  black  in  color,  airless,  and  on  pressure  exudes  only  a  small 
amount  of  bloody  fluid.  Infarcts  are  usually  hard  and  their  boundaries 
sharply  defined,  thus  differing  from  ordinary  hemorrhages  into  the 
pulmonary  tissue  from  ruptured  vessels.  The  neighboring  tissue  may 
be  edematous.  A  zone  of  hyperemia  may  also  bound  the  infarcted 
area,  its  brighter  color  in  sharp  contrast  to  the  dark  red  of  the  infarct 
itself. 

On  microscopic  examination  of  a  recent  hemorrhagic  infarct  the 
capillaries,  alveoli,  interstitial  tissue,  and  bronchi  are  found  crowded 
with  red-blood  corpuscles.  A  small  amount  of  fibrin  may  be  present, 
but  this  is  usually  more  abundant  in  older  infarcts.  The  capillaries 
also  contain  hyaline  thrombi.  In  older  infarcts,  and  especially  toward 
the  central  part  of  the  involved  region,  the  alveolar  walls  almost 
constantly  show  coagulation  necrosis,  as  Willgerodt1  emphasized. 
Disintegration  of  the  red  cells  may  also  take  place. 

It  is  probable  that  in  some  cases  in  which  the  pulmonary  infarction 
involves  only  a  small  area  the  circulation  may  be  at  least  partially 
reestablished.  Necrosis  of  tissue,  however,  is  an  almost  invariable 
result,  and  complete  resolution  can  hardly  be  expected.  Organization 
takes  place,  the  infarct  is  finally  converted  into  connective  tissue  and 
remains  as  a  puckered  and  pigmented  scar. 

Infection  of  the  infarcted  area  may  arise  from  infected  emboli  or 
by  extension  from  the  bronchi  or  lung.  Suppuration,  extensive  necrosis, 
abscess  formation,  and  gangrene  may  then  occur.  A  sequestrum  may 
form  in  the  infarcted  area.  Multiple  pulmonary  abscesses,  interstitial 
pneumonia,  and  empyema  may  follow. 

Symptoms  and  Course. — Pulmonary  embolism  would  less  often 
occur  if  it  were  always  possible  to  recognize  venous  thrombosis. 
Involvement  of  the  superficial  veins  of  the  extremities  is  usually  easily 
determined  from  the  presence  of  pain,  palpable  and  tender  veins,  and 
edema.  Dilatation  of  veins  tributary  to  the  venous  channels  suspected 
of  thrombosis  may  be  suggestive.  Unfortunately,  thrombosis  of  deep 
veins  may  be  unaccompanied  by  any  symptoms  whatever.  Mahler2 
regards  a  step-like  rise  of  the  pulse,  the  temperature  still  remaining 
low,  as  an  important  sign  of  thrombosis  and  most  marked  following 
pulmonary  embolism.  This  sign  is  at  times  of  value,  but  is  often  absent, 
and  its  interpretation  difficult  from  the  presence  of  complications. 

It  is  convenient  for  purposes  of  description  to  consider  the  symptoms 

1  Ueber  die  hamorrh.  Inf.  d.  Lungen,  Arb.  aus  d.  path.  Inst,  in  Gottingen,  Berlin, 
1893,  pp.  100-120. 

2  Thrombose,  Lungenembolie  und  plotzlicher  Tod,  in  Leopold,  Geburtshilfe  und 
Gynakologie.    Arbeiten  aus  der  kgl.  Frauenklinik  im  Dresden,  1895,  Bd.  ii,  pp.  72-120. 


336  DISEASES  OF  THE  LUNGS 

of  (1)  pulmonary  embolism,  or  the  "embolic  act,"  as  Gerhardt1  termed 
it,  and  (2)  pulmonary  infarction,  separately. 

1.  Pulmonary  Embolism. — Various  factors  have  a  bearing  on  the 
clinical  features.  Sudden  and  complete  occlusion  of  a  pulmonary 
artery  is  followed  by  more  obvious  and  more  serious  results  than  gradual 
and  incomplete  closure.  The  symptoms  naturally  vary  also  with  the 
number  of  the  emboli.  Embolism  of  infected  material  has  little  bearing 
on  the  immediate  symptoms,  but  exerts  an  important  influence  on  the 
subsequent  course.  The  patient's  condition  is  a  factor.  Embolism 
is  of  graver  consequence  in  those  already  weakened  by  disease,  and 
especially  in  those  with  cardiac  disease.  The  clinical  picture  also 
presents  important  differences  according  to  the  size  of  the  occluded 
vessels  and  the  nature  of  the  embolus.  A  division  is  therefore  made 
into  (a)  embolism  of  the  pulmonary  artery  or  its  main  divisions,  (b) 
of  medium-sized  and  smaller  branches,  and  (c)  capillary  embolism. 
In  the  following  pages,  embolism  of  blood-clot  is  discussed.  Air 
embolism,  fat  embolism,  mercury  embolism,  cell  embolism,  and  hydatid 
embolism  will  be  considered  under  separate  headings. 

(a)  Embolism  of  the  Pulmonary  Artery  or  its  Main  Divisions. — 
The  sudden  and  complete  occlusion  of  the  pulmonary  artery,  both  its 
main  divisions  or  their  branches,  is  followed  by  death  which  occurs 
at  once  or  within  one  to  two  minutes.  Prolongation  of  life  beyond 
this  period  is  probably  due  to  incomplete  occlusion.  Trendelenburg2 
in  9  cases  noted  an  immediately  fatal  termination  in  2,  and  an  interval 
of  ten,  fifteen  to  twenty,  about  thirty,  thirty  to  thirty-five,  about 
fort}'  minutes  and  one  hour  before  death  in  the  remaining  7  cases 
with  embolism  of  the  pulmonary  artery.  Of  4  cases  in  the  Massa- 
chusetts General  Hospital  series,  the  fatal  ending  took  place  in  ten, 
fifteen,  twenty-five,  and  forty-five  minutes  respectively. 

Occlusion  of  one  main  division  may  be  less  rapidly  fatal.  In  three 
cases  in  this  series,  life  wTas  prolonged  for  forty-five  minutes,  nine  hours, 
and  two  days  respectively.  In  exceptional  instances,  life  may  last  for 
an  even  longer  period.  Plart3  has  reported  two  cases  with  total  occlu- 
sion of  a  main  division  of  the  pulmonary  artery  in  which  an  advanced 
organization  indicated  a  long  previous  duration. 

In  the  rapidly  fatal  cases,  death  may  actually  be  the  first  symptom. 
It  may  be  preceded  merely  by  a  groan  or  an  outcry.  In  other  instances 
the  patient  is  suddenly  overcome  with  a  sense  of  oppression  and  pre- 
cordial distress,  the  face  is  pale  or  pale  and  cyanotic,  the  pulse  rapid, 
weak,  and  irregular  or  imperceptible,  and  death  takes  place  in  coma 
or  convulsions.  If  the  course  is  more  protracted,  the  sudden  onset 
of  thoracic  oppression,  intense  dyspnea,  orthopnea,  distress,  or  pain 
referred  to  the  shoulders,  the  chest,  or  upper  abdomen,  extreme  appre- 

1  C.  Gerhardt,  Der  Hamorrhagischc  Infarkt.,  Volkmann's  Klinische  Vortriigc,  4th  S., 
PI).  91-120. 

2  Deut.  Gesellsch.  f.  Chir.,  Berlin,  Verhandl.,  1908,  vol.  xxxvii. 

3  Deut.  Arch.  f.  klin.  Med.,  1905,  lxxxiv,  449. 


THROMBOSIS,  EMBOLISM  AND  INFARCTION  337 

hension,  restlessness,  cold  and  clammy  sweats,  chills,  syncope,  delirium, 
involuntary  urine  and  feces,  and  convulsions  may  be  noted.  Con- 
sciousness may  be  retained  throughout.  It  may  be  lost  at  first,  to 
be  regained  later  with  an  improvement  of  the  other  symptoms.  An 
interval  of  comparative  comfort  may  be  followed  by  a  recurrence  of 
symptoms.  In  one  of  the  hospital  cases  the  patient  died  in  the  last 
of  three  attacks,  occurring  within  forty-five  minutes.  The  pulmonary 
artery  was  occluded  by  a  single,  coiled  clot  45  cm.  long.  The  reappear- 
ance or  exaggeration  of  symptoms  may  be  due  to  displacement  of  a 
mass  insecurely  fixed,  to  fresh  emboli,  reflex  causes  or  thrombus  form- 
ation about  the  embolus.  The  contrast  between  the  intensity  of  the 
dyspnea  and  the  freedom  with  which  air  enters  or  leaves  the  lung  may 
be  a  striking  feature.  During  the  attack,  examination  may  show  pallor 
followed  by  intense  cyanosis.  The  cervical  veins  may  be  markedly 
dilated,  and  in  some  instances  show  independent  pulsation.  The  pulse 
is  usually  rapid,  of  small  volume  and  low  tension,  and  may  be  irregular 
or  imperceptible.  An  increased  area  of  cardiac  dulness  to  the  right 
of  the  sternum  and  a  displacement  of  the  apex  beat  to  the  left,  from 
dilatation  of  the  right  side,  may  be  determined.  The  pulmonic  second 
sound  may  be  accentuated.  The  circulatory  disturbances  are  largely 
due  to  the  blocking  of  the  pulmonary  circuit  with  consequent  anemia 
of  the  arterial,  congestion  of  the  venous  system,  and  embarrassment  of 
the  right  heart. 

Distinctive  physical  signs  on  the  part  of  the  lung  are  lacking. 
Pulmonary  edema  may  ensue  in  protracted  cases.  Litten1  called 
attention  to  a  rough  murmur,  and  under  favorable  circumstances  also 
a  thrill,  coincident  with  and  outlasting  systole  for  a  variable  period. 
The  murmur  is  heard  in  the  region  of  the  upper  border  of  the  third 
left  rib  or  second  left  costal  cartilage,  may  also  be  audible  over  the 
whole  anterior  part  of  the  thorax  and  in  the  interscapular  region  at 
about  the  level  of  the  third  dorsal  vertebra.  The  narrowing  of  the 
pulmonary  blood-stream  accounts  for  it.  Litten  heard  it  in  4  cases, 
in  which  embolic  occlusion  of  the  pulmonary  artery  was  found  at 
autopsy.  The  diagnosis  was  made  during  life  in  three.  Murmurs 
due  to  narrowing  of  the  pulmonary  blood-stream  from  other  causes 
have  been  noted  by  Immermann,2  Aufrecht3  and  Frankel.4  Litten 
made  the  further  interesting  observations  in  one  case  of  a  double 
apex  beat  and  double  first  sound,  probably  due  to  increased  resistance 
in  the  narrowed  pulmonary  circuit. 

In  cases  in  which  the  patient  immediately  loses  consciousness  and 
dies  in  syncope,  death  is  usually  ascribed  to  cerebral  anemia.  Inter- 
ference with  the  coronary  circulation  is  also  a  possible  explanation. 
The  experiments  of  Russell  and  Brodie,5  and  Capps  and  Lewis6  on 

1  Berl.  klin.  Woch.,  1882,  Nos.  28  and  29. 

2  Deut.  Arch.  f.  klin.  Med.,  1869,  Bd.  v,  p.  235.  3  Ibid.,  1876,  Bd.  xviii,  p.  629. 
4  Spez.  Path.  u.  Ther.  der  Lungenkrankheiten,  1904,  p.  512. 

6  Jour,  of  Phys.,  1900-01,  vol.  xxvi. 
6  Amer.  Jour.  Med.  Sei.,  December,  1907. 
22 


338  DISEASES  OF  THE  LINGS 

pulmonary  and  pleural  reflexes  suggest  that  reflex  cardiac  inhibition 
may  also  be  a  factor.  In  the  more  protracted  cases,  in  which  dyspnea 
is  a  striking  feature,  death  has  been  ascribed  to  asphyxia. 

Pulmonary  infarction  is  relatively  uncommon  as  a  consequence  of 
embolism  of  the  pulmonary  artery  or  its  main  divisions.  In  the  cases 
in  which  it  occurs,  the  plugging  in  the  artery  or  its  main  branches  may 
he  incomplete,  and  a  plug  in  a  smaller  branch  may  be  responsible  for 
the  infarction. 

{!>)  Embolism  of  Medium-sized  and  Smaller  Branches  of  the  Pul- 
monary Artery. — The  symptoms  following  total  occlusion  of  all  branches 
from  one  of  the  main  divisions  of  the  pulmonary  artery  do  not  differ 
from  those  described  above.  The  plugging  of  single  branches  of  one 
of  the  main  divisions  may  also  be  followed  by  similar  but  usually 
less  intense  symptoms.  In  patients  already  weakened  by  disease, 
the  symptoms  may  be  marked  and  the  termination  fatal.  Embolism 
of  medium  and  smaller  pulmonary  arteries  is  more  often  latent  than 
obvious.  It  is  more  common  and  of  special  interest  because  of  its 
important  relation  with  pulmonary  infarction. 

(c)  Capillary  Embolism. — The  lodgement  of  foreign  substances  in 
the  finer  ramifications  of  the  pulmonary  arteries  and  the  pulmonary 
capillaries  gives  rise  to  symptoms  of  embolism  only  when  there  is 
mechanical  obstruction  of  a  large  territory.  Air  embolism,  fat 
embolism,  mercury  embolism,  and  cell  embolism  may  be  mentioned 
as  examples  of  this  type. 

So-called  parasitic  emboli  embrace  the  largest  group.  Their  invasion 
of  the  lungs  is  unaccompanied  by  symptoms  of  embolism,  and  they 
are  of  chief  importance  because  of  the  pulmonary  conditions  to  which 
they  give  rise.  Infected  venous  thrombi,  and  endocardial  vegetations 
may  transport  bacteria  into  the  lung  with  consequent  metastatic 
pulmonary  abscesses.  Invasion  of  the  venous  system  by  tubercle 
bacilli,  actinomyces,  and  streptothrix  may  cause  secondary  pulmonary 
infection. 

The  transport  of  malignant  tumor  cells  may  give  rise  to  metastatic 
new  growths  in  the  lungs. 

2.  Infarction. — This  is  often  latent  and  discovered  only  at  autopsy. 
This  is  more  likely  in  patients  already  seriously  ill,  as  with  cardiac 
disease  and  broken  compensation.  The  symptoms  of  embolism  may 
accompany  the  attack,  but  this  is  unusual,  as  infarction  is  more  par- 
ticularly a  feature  of  occlusion  of  the  smaller  pulmonary  vessels. 

Pain  is  the  most  constant  and  usually  the  first  symptom  of  infarc- 
tion. It  resembles  that  from  ordinary  pleurisy,  is  usually  unilateral, 
but  may  occur  on  both  sides  of  the  chest  and  is  then  probably  due  to 
simultaneous  infarction  of  both  lungs.  It  may  at  times  be  felt  in  the 
shoulder  or  upper  abdomen.  The  pain  may  be  sudden  and  severe  in  its 
onset,  or  begin  as  a  slight  discomfort  on  long  breath  or  cough,  gradually 
increasing  in  intensity  during  the  first  twenty-four  hours.  It  may  be 
the  only  symptom.     A  chill  or  chilliness  may  accompany  the  pain. 


THROMBOSIS,  EMBOLISM  AND  INFARCTION  339 

The  breathing  is  likely  to  be  rapid.  There  may  be  dyspnea  from 
restricted  respiration  and  a  slight  dry  cough.  During  the^  first  part 
of  the  attack  the  temperature  is  usually  normal  and  examination  of 
the  lungs  negative. 

The  expectoration  of  blood  is  an  important  symptom,  but  may  be 
absent.  When  it  occurs,  it  usually  begins  after  the  onset  of  pain. 
Its  appearance  is  usually  delayed  for  a  few  hours,  and  it  may  not 
come  for  two  to  three  days.  In  typical  and  uncomplicated  cases,  it 
consists  of  homogeneous,  viscid,  tenacious,  dark  red  masses  of  vari- 
able size.  The  tenacious  quality  is  due  to  an  admixture  of  mucus. 
The  character  of  the  sputum  alone  may  be  very  suggestive  of 
infarction.  The  total  amount  seldom  exceeds  a  few  drams  in  twenty- 
four  hours.  The  expectoration  of  pure  blood  was  never  observed  by 
Gerhardt1  nor  was  it  seen  in  any  of  my  cases.  The  expectoration  of 
large  amounts  of  pure  blood  was  noted  by  Laennec,  but  I  judge  from 
his  description  that  he  confused  other  forms  of  hemoptysis  with  that 
from  infarction.  In  one  of  Frankel's  patients  the  daily  amount  of 
dark  red  sputum  repeatedly  reached  300  to  500  c.c.  If  the  infarction 
breaks  down  with  the  formation  of  cavities,  copious  bleeding  may 
occur.  In  long-continued  and  complicated  cases,  bloody  masses  of 
sputum  may  be  mixed  with  mucopurulent  material.  The  expectora- 
tion of  blood  may  continue  for  weeks,  but  in  favorable  cases  gradually 
diminishes  in  amount.  The  sputum  and  also  the  breath  may  have 
a  slightly  musty  or  foul  odor,  even  in  cases  which  ultimately  progress 
favorably.  On  microscopic  examination,  red-blood  corpuscles  and 
pigmented  alveolar  cells  may  be  found.  The  blood  pigment  is  in  the 
form  of  amorphous  brownish  masses  or  crystals  of  hematoidin.  The 
absence  of  bacteria  in  the  stained  specimens  may  be  a  striking  feature, 
upon  which,  however,  too  much  reliance  should  not  be  placed. 

Physical  signs  are 'often  lacking,  because  of  the  small  size  of  the 
infarct,  in  rare  instances  because  of  its  central  position.  When  present, 
they  usually  appear  coincident  with  or  soon  after  the  hemoptysis  and 
are  more  often  found  over  the  inferior  and  posterior  or  lateral  parts  of 
the  lung.  According  to  Gerhardt,  the  right  side  between  the  angle 
of  the  scapula,  the  vertebral  column  and  the  diaphragm  is  most  often 
affected.  In  rare  instances  the  apex  may  be  involved.  The  signs  are 
those  of  pulmonary  consolidation  and  are  not  distinctive  of  infarction. 
The  interspaces  may  be  narrowed  on  the  affected  side.  The  respiratory 
excursion  of  the  involved  lung  may  be  diminished.  Over  the  infarct, 
dulness,  fine  or  medium,  consonating  or  non-consonating  rales,  dimin- 
ished vesicular  or  bronchial  breathing,  increased  voice,  whisper  and 
tactile  fremitus  may  be  observed.  The  dulness  has  often  been  noted 
to  have,  a  tympanitic  quality,  the  explanation  of  which  is  not  clear. 
It  has  been  ascribed  to  edema  or  relaxation  of  the  neighboring  lung 
or  (and  more  plausibly)  to  the  vibration  of  air  in  the  open  bronchi. 

1  Klin.  Vortrage,  Volkmann,  4  S.,  xci-cxx,  730. 


340 


DISEASES  OF   THE  LUNGS 


A  pleural  friction  rub  is  not  uncommon  and  may  be  heard  over  a  much 
larger  area  than  the  apparent  size  of  the  infarct  itself.  With  small 
infarcts  the  pleural  may  be  the  only  manifestations.  It  cannot  be 
stated  how  large  an  infarct  must  be  to  give  rise  to  physical  signs. 
Gerhardt  believed  that  in  the  majority  of  all  cases  in  which  it  measures 
from  one  to  four  cubic  inches  (the  size  of  a  nut  to  that  of  an  egg), 
obvious  dulness  may  be  expected.  The  prevailing  subpleural  position 
of  the  base  of  infarcted  areas  and  the  frequent  edema  and  hyperemia 
of  the  neighboring  lung  favor  its  detection.  It  has  nevertheless  hap- 
pened in  the  experience  of  many  observers  that  infarcts  of  considerable 
size,  undetected  during  life,  have  been  found  at  autopsy.  To  judge 
from  the  hospital  cases,  pulmonary  infarcts  seldom  lead  to  other  than 
fibrinous  inflammation  of  the  pleura.  In  most  cases  complicated  by 
more  than  small  amounts  of  pleural  fluid,  coincident  cardiac  or  other 
disease  suggests  another  explanation  for  the  pleural  effusion. 

The  temperature  may  be  normal  throughout.  Moderate  fever, 
however,  is  not  uncommon  and  usually  begins,  not  with  the  pain,  but 
with  or  shortly  after  the  hemoptysis. 

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Febrile  reaction  following  pulmonary  embolism.  The  source  of  the  embolus  could 
not  be  discovered  until  ten  days  later  when  phlebitis  of  the  left  leg  became  manifest. 
The  second  period  of  elevated  temperature  is  due  to  the  phlebitis.     (P.  C.) 


The  further  course  of  pulmonary  infarction  depends  more  upon  the 
seriousness  of  the  underlying  disease  than  upon  the  infarction  itself, 
which  is  often  only  an  incident  in  an  otherwise  serious  affection. 
Numerous  infarcts  or  those  of  large  size  may  be  a  contributing  or  even 
a  principal  cause  of  death.     Small  and  uninfected  infarcts  usually 


THROMBOSIS,  EMBOLISM  AND  INFARCTION  341 

run  a  favorable  course.  The  temperature  gradually  falls.  Bloody 
sputum  and  signs  of  pulmonary  solidification  usually  persist  for  a  longer 
period,  but  ordinarily  they,  too,  subside  in  the  course  of  a  few  weeks. 
Examination  may  then  fail  to  disclose  evidence  of  the  previous  trouble 
in  the  lung  or  pleura.  The  patient  (P.  C),  whose  chart  is  shown  above, 
has  safely  passed  through  five  attacks  of  embolic  pulmonary  infarction 
arising  from  thrombosis  of  the  saphenous  veins.  All  his  attacks  have 
been  accompanied  by  symptoms  of  pleurisy,  three  by  hemoptysis, 
and  two  by  evidence  of  pulmonary  consolidation.  Yet  in  spite  of  this, 
the  lungs  are  negative  and  the  pleural  sacs  free,  as  indicated  by  a  wide 
excursion  of  the  diaphragm  shadow.  The  heart  is  negative,  with  a  rate 
of  about  80  beats  per  minute  at  rest,  but  exertion  is  followed  by  tachy- 
cardia which  may  amount  to  100,  110  and  even  120  beats  per  minute. 
An  infected  clot  gives  rise  to  more  serious  disturbances.  Pneumonic 
infiltration  may  arise  in  the  neighboring  lung.  Abscess  formation 
or  gangrene  may  develop  at  the  site  of  the  infarct.  In  the  presence 
of  such  pulmonary  complications,  the  sputum  changes  its  character, 
and  in  addition  to  blood  from  the  infarct,  contains  pus  which  may  be 
foul,  and  elastic  tissue.  Empyema  or  pneumothorax  may  complicate 
the  destructive  pulmonary  changes. 

Diagnosis. — Thrombosis  and  embolism  of  the  pulmonary  artery 
or  its  branches  can  hardly  be  differentiated  clinically.  It  is  probable, 
as  already  mentioned,  that  in  the  majority  of  cases  in  which  plugging 
of  the  pulmonary  arteries  occurs,  the  occlusion  is  due  to  embolism 
rather  than  to  thrombosis.  The  apparent  absence  of  thrombosis 
does  not  exclude  embolism,  for  the  thrombosis  may  be  undemon- 
strable  in  an  inaccessible  vein  or  latent  even  in  the  extremities. 

Embolism  may  be  suspected  when  sudden  and  unexpected  death 
or  suggestive  symptoms  occur  in  the  presence  of  a  recognized  throm- 
bosis of  a  systemic  vein,  or  in  the  course  of  diseases  or  conditions  known 
to  be  frequently  complicated  by  venous  thrombosis.  The  suddenness 
of  onset,  the  intensity  of  the  dyspnea  without  evidence  of  respiratory 
obstruction,  distress  rather  than  pain,  pallor  followed  by  cyanosis, 
dilated  and  at  times  pulsating  cervical  veins,  signs  of  cardiac  weakness 
or  dilatation  and  the  appearance  of  a  murmur  over  the  base,  such  as 
that  described,  may  be  mentioned  as  more  or  less  typical  features. 

The  condition  may  be  confused  with  coronary  artery  disease  in 
which,  although  death  may  occur  in  the  first  paroxysm,  there  will 
usually  be  a  history  of  previous  attacks.  Pain  is  a  more  prominent 
symptom,  and  dyspnea  and  cyanosis  are  less  often  present  to  such  a 
degree  as  in  pulmonary  embolism.  An  acute  cardiac  failure  in  the 
course  of  chronic  myocardial  or  valvular  disease  offers  the  greatest 
difficulty  from  the  frequency  with  which  such  a  condition  is  complicated 
by  pulmonary  embolism.  The  condition  known  as  cardiac  asthma 
may  closely  simulate  pulmonary  embolism,  and  in  some  instances 
cannot  be  distinguished  from  it.  Here,  too,  the  previous  history  will 
be  of  assistance,  but  it  is  probable  that  slowing  of  the  pulmonary 


342  DISEASES  OF  THE  LUNGS 

circulation  is  largely  responsible  for  the  symptoms  in  both  conditions. 
When  embolism  occurs  as  a  late  complication,  not  only  of  cardiac 
disease  but  also  of  other  intrathoracic  conditions  accompanied  by 
dyspnea,  there  may  be  no  distinctive  symptoms,  and  the  first  intima- 
tion of  its  occurrence  come  at  the  autopsy  table. 

The  clinical  picture  of  pulmonary  infarction  is  variable.  Its  most 
suggestive  features  may  be  thus  summarized :  The  attack  begins  with 
pleural  pain,  usually  followed  after  an  interval  by  bloody  sputum  of 
a  peculiar  character.  The  hemoptysis  is  in  turn  accompanied  or  suc- 
ceeded by  dry  pleurisy  and  pulmonary  consolidation  with  or  without 
fever.  Attention  to  the  order  in  which  the  symptoms  appear  may 
suggest  the  diagnosis.  Owing  to  the  usual  small  size  of  the  arteries 
affected,  preceding  symptoms  of  embolism  are  often  lacking.  In  an 
attack  of  pleurisy  alone  in  the  course  of  such  conditions  as  give  rise 
to  embolism,  infarction  should  be  suspected.  In  rare  instances  the 
pleurisy  may  be  apparently  primary.  Such  an  attack  during  the  puer- 
perium  is  very  suggestive  of  infarction.    Tuberculosis  must  be  excluded. 

Pulmonary  tuberculosis  may  simulate  pulmonary  infarction.  A 
family  history  of  the  disease  or  opportunity  for  contagion,  the  expec- 
toration of  bright  red  and  clear  blood  rather  than  dark  red  and  tena- 
cious masses,  the  absence  of  coincident  pleurisy,  prevalent  involvement 
of  the  apices  rather  than  the  bases  of  the  lungs,  and  the  presence  of 
tubercle  bacilli  in  the  sputum,  may  be  distinguishing  features.  If  neces- 
sary, tuberculin  may  be  used.  Nevertheless  the  differentiation  is  not 
always  easy.  Bloody  sputum  from  tuberculous  processes  may  re- 
semble that  from  an  area  of  infarction.  Pleurisy  may  accompany  and 
fever  may  follow  the  hemoptysis  in  both  conditions.  Tubercle  bacilli 
are  likely  to  be  absent  from  the  bloody  sputum  of  tuberculous  patient 
early  in  the  disease.  The  order  in  which  the  different  features  appear 
in  infarction,  the  site  and  gradual  disappearance  of  the  pulmonary 
lesion  in  favorable  cases,  and  the  finding  of  venous  thrombosis  as  a 
source  of  emboli  will  usually  establish  the  diagnosis.  The  exclusion 
of  lobar  pneumonia  by  the  more  constant  initial  chill,  more  immediate 
rise  and  more  rapid  fall  of  the  fever,  rusty  sputum  and  more  extensive 
yet  more  rapidly  resolving  pulmonary  involvement  is  usually  not 
difficult.  The  embolic  character  of  a  septic  pneumonia,  however, 
may  be  difficult  or  even  impossible  of  detection,  although  it  may  be 
suspected  if  a  primary  source  for  venous  infection  can  be  found.  The 
bloody  sputum  from  malignant  tumors  of  the  lung  may  closely  resemble 
that  from  pulmonary  infarcts,  but  pleural  pain  coincident  with  its 
appearance  is  unusual,  a  primary  tumor  may  be  found  elsewhere,  and 
the  further  course  of  the  disease  is  not  that  of  infarction.  It  should 
be  remembered  that  pulmonary  infarcts  are  not  very  uncommon  as  a 
complication  of  new  growths,  and  unless  careful  account  is  taken  of  the 
progress  of  the  symptoms,  may  be  mistaken  for  secondary  malignant 
disease  of  the  lung.  Hemoptysis  may  occur  as  a  symptom  of  erhino- 
coccus  cysts  of  the  lung.    It  is  not  uncommon  before  as  well  as  after 


THROMBOSIS,  EMBOLISM  AND  INFARCTION  343 

rupture,  and  pleuritis  is  a  frequent  early  symptom.  In  Gerhardt's1 
case,  with  bloody  sputum,  flatness  and  diminished  breathing  below  the 
right  nipple,  infarction  was  suspected  until  the  sputum  became  more 
fluid  and  more  abundant  and  was  found  to  contain  cyst  membrane. 
Booklets  may  also  be  found  in  the  sputum.  In  some  cases  echinococcus 
cysts  elsewhere  will  suggest  the  diagnosis.  Chronic  passive  congestion 
consecutive  to  cardiac  disease  is  a  common  cause  of  bloody  streaks 
or  a  frothy  bloody  mucus,  which  in  the  absence  of  pleural  pain  and 
signs  of  consolidation  should  not  give  rise  to  confusion. 

Prognosis. — This  varies  with  the  number  and  size  of  the  occluded 
vessels,  the  completeness  of  the  closure,  the  character  of  the  embolus 
and  the  previous  condition  of  the  patient.  It  may  be  said  in 
review  that  the  sudden  and  complete  occlusion  of  the  pulmonary 
artery  itself,  one  of  its  main  divisions  or  their  branches  is  almost 
invariably  fatal,  regardless  of  the  patient's  previous  condition. 
The  prognosis  of  embolism  of  smaller  vessels  is  apparently  usually 
good  so  far  as  immediate  consequences  are  concerned,  provided 
the  pulmonary  circulation  is  unimpaired.  It  may,  however,  lead  to 
infarction.  Occlusion  of  these  vessels  complicating  existing  cardiac 
weakness  may  be  fatal  and  is  very  likely  to  lead  to  infarction.  Large 
infarcts  may  be  fatal.  Small  and  medium  sized  infarcts  frequently 
end  in  recovery,  but  here  also  the  general  condition  of  the  patient 
and  the  presence  or  absence  of  infection  of  the  affected  region  are 
important  factors. 

Treatment.— The  utmost  care  should  be  taken  to  avoid  detachment 
of  emboli  from  a  recognized  or  suspected  venous  thrombus.  The 
patient  should  be  warned  of  the  danger  of  pulmonary  embolism  and 
cautioned  also  against  sudden  movements,  straining  at  stool  or  violent 
coughing.  He  should  be  in  bed,  with  the  affected  part  absolutely  at 
rest.  If  an  extremity  is  involved,  it  should  be  immobilized.  The  length 
of  time  which  must  elapse  before  the  danger  is  past,  varies  with  the 
severity  of  the  process  and  cannot  be  definitely  stated.  Disappear- 
ance of  local  tenderness,  diminishing  edema  and  absence  of  fever  are 
favorable  indications.  In  cases  which  progress  satisfactorily,  absolute 
quiet  for  a  month  to  six  weeks  may  usually  be  considered  a  safe  limit. 
Customary  activities  should  only  be  gradually  resumed. 

In  cases  of  pulmonary  embolism  with  serious  symptoms  there  is 
always  a  chance  that  the  plug  rides  on  the  bifurcation  of  the  pulmonary 
artery  or  only  incompletely  occludes  a  vessel.  Displacement  of  such 
a  clot  may  be  fatal.  The  patient  should  therefore  be  quietly  at  rest 
in  bed,  and  every  unnecessary  movement,  even  talking,  avoided. 
Physical  examination,  if  made  at  all,  should  be  limited  to  accessible 
parts  of  the  chest.  Morphia  may  be  given  for  pain  or  distress.  Frankel 
recommends  hot  hand-baths  and  sinapisms  to  the  chest  and  calves 
to  dilate  the  peripheral  vessels  and  delay  the  venous  return.     Other 

1  Loc.  cit.,  p.  735. 


344  DISEASES  OF  THE  LUNGS 

than  such  simple  measures  may  do  more  harm  than  good.  Cardiac 
stimulation  is,  if  possible,  to  be  avoided,  since  it  may  start  a  fresh 
embolus  or  transport  a  clot  into  a  more  dangerous  site.  The  fre- 
quency with  which  plugging  of  the  pulmonary  arteries  is  associated 
with  right-sided  cardiac  thrombosis,  suggests  great  caution  in  pursuing 
other  than  such  an  expectant  policy. 

Trendelenburg1  recommends  the  operative  removal  of  emboli  from 
the  pulmonary  artery.  This  has  been  accomplished  in  4  cases,2  but 
without  preventing  a  fatal  termination.  Siever's  patient  lived  fifteen 
hours,  Kriiger's  five  and  a  quarter  days  after  the  operation.  The 
number  of  cases  in  which  surgical  interference  can  be  considered  is 
relatively  small,  and  in  view  of  the  difficulty  of  diagnosis  and  the 
dangers  of  the  operation,  the  chances  for  recovery  at  present  are 
probably  better  without  than  with  operation.3 

With  -pulmonary  infarction,  the  relief  of  pain  is  usually  the  chief 
indication.  Absolute  rest  in  bed  will  not  only  diminish  the  pain,  but 
also  lessen  the  danger  of  other  infarcts  from  fresh  emboli.  Fixation 
of  the  side,  an  ice-bag,  or  hot  water  bottle  may  be  sufficient.  If  not, 
morphin  may  be  given.  Examination  of  the  lungs  should  be  made, 
but  with  care  not  to  disturb  the  patient.  The  hemoptysis  does  not 
require  treatment.  The  blood  effused  into  the  bronchi  must  be  expec- 
torated. If  it  is  not  and  the  infarct  has  become  infected,  the  aspira- 
tion of  infected  blood  into  sound  parts  of  the  lung  may  give  rise  to 
bronchopneumonia.  It  is  doubtful  if  the  various  styptics  commonly 
recommended  have  any  control  over  hemoptysis,  and  if  they  did, 
it  would  be  inadvisable  to  use  them.  The  administration  of  calcium 
salts  to  increase  the  coagulability  of  the  blood  may  do  harm  by  induc- 
ing more  extensive  thrombus  formation  in  the  affected  vessels.  Pleural 
effusions  complicating  pulmonary  infarction  may  be  treated  in  general 
on  the  same  principles  governing  the  treatment  of  similar  effusions 
from  other  causes.     An  empyema  should  be  opened  and  drained. 

1  Operativ.  Behandl.  d.  Emb.  d.  Lungenarterie,  Deut.  Gesellsch.  f.  Chir.,  Berlin, 
Verhandl.,  1908,  vol.  xxxvii. 

2  Trendelenburg,  ibid.,  and  Deut.  med.  Woch.,  July  2,  1908,  No.  27;  Sievers,  Deut, 
Zeit.  f.  Chir.,  1908,  p.  93;  Kriiger,  Zeit.  f.  Chir.,  1909,  No.  21,  p.  757. 

3  The  skin  is  incised  from  the  sternal  margin  for  a  distance  of  about  10  cm.  along 
the  second  rib,  and  along  the  sternal  margin,  perpendicular  to  this  incision,  from  the 
insertion  of  the  first  to  that  of  the  third  rib.  The  two  triangular  flaps  of  skin  are  laid 
back  and  the  sternal  portion  of  the  second  rib  resected.  The  pleura  and  the  pericardium 
are  opened  with  care  not  to  wound  the  internal  mammary  artery  or  the  phrenic  nerve. 
By  means  of  a  sound,  a  piece  of  rubber  tubing  is  passed  behind  the  aorta  and  the  pul- 
monary artery,  through  the  pericardial  sinus.  With  this  the  vessels  can  be  drawn  for- 
ward and  partially  or  completely  compressed.  The  pulmonary  artery  is  opened,  the 
embolus  withdrawn,  and  the  venous  opening  temporarily  closed  with  forceps.  The 
arterial  opening  is  sutured  above  the  blades  of  the  closed  forceps,  with  fine  silk,  including 
the  intima.  Cardiac  pulsations  may  disturb  this  procedure,  but  they  may  be  controlled 
for  a  few  seconds  at  a  time  by  constriction  of  the  vessels  with  the  rubber  tube  still  left 
in  place.  Special  instruments  are  used.  They  should  be  constantly  ready  for  use. 
Artificial  pneumothorax  on  the  operated  side  is  a  disadvantage  which  might  be  over- 
come by  the  use  of  positive  or  negative  pressure  apparatus.  Their  inconvenience  and 
the  time  consumed  in  preparation  are  as  yet  insuperable  difficulties. 


THROMBOSIS,  EMBOLISM  AND  INFARCTION  345 

Large  serofibrinous  effusions  or  those  causing  pressure  symptoms 
should  be  evacuated,  but  small  or  medium  serofibrinous  effusions  may 
well  be  allowed  to  remain  for  a  time  at  least  for  fear  of  dislodging 
pulmonary  thrombi  by  their  removal  and  in  the  hope  that  they  will 
be  absorbed.  This  applies  particularly  to  the  effusions  which,  from 
their  appearance  after  the  infarction,  seem  to  arise  in  consequence  of  it. 
In  the  cases  in  which  the  relation  is  reversed  and  the  pulmonary 
embolism  complicates  the  pleural  effusion,  a  more  common  condition, 
I  believe,  it  is  probable  that  the  pleural  effusion  has  played  an  impor- 
tant part  in  giving  rise  to  the  thrombus  from  which  the  embolus  has 
come.  Judgment  as  to  the  best  course  to  pursue  in  these  cases  is  diffi- 
cult as  one  has  to  weigh  on  the  one  hand  the  danger  of  more  extensive 
thrombosis  if  the  fluid  is  allowed  to  remain  and  the  possible  detach- 
ment of  fresh  emboli  by  its  removal.  In  such  cases,  if  the  symptoms 
from  the  effusion  are  not  urgent,  it  is  probably  best  to  wait,  keeping 
the  patient  meanwhile  absolutely  at  rest,  in  the  hope  that  loosely 
attached  thrombi  may  become  fixed. 

Air  Embolism.1 — The  first  recognition  of  air  embolism  during  opera- 
tion as  a  cause  of  death  appears  to  have  been  made  by  Beauchene  and 
reported  in  1821  by  Majendie.2  Many  cases  have  since  been  reported. 
The  cause  of  death  has  been  the  subject  of  much  discussion  and 
experimentation . 

Atmospheric  air  may  enter  the  veins  in  the  course  of  operations 
about  large  venous  trunks,  as  in  the  neck,  about  the  shoulder,  the 
upper  thoracic  region,  and  the  cerebral  sinuses.  It  may  take  place 
through  the  uterine  veins,  after  detachment  of  a  placenta  previa  or 
following  intrauterine  injections  for  the  production  of  abortion.  Air 
embolism  has  followed  attempts  to  produce  artificial  pneumothorax 
in  a  number  of  cases.  (See  Artificial  Pneumothorax.)  Welch  and 
Flexner3  have  called  attention  to  the  possibility  of  mistaking  gas  for- 
mation after  infection  with  the  bacillus  aerogenes  capsulatus  for  air 
embolism,  and  unless  a  bacteriologic  examination  is  made  death  can 
safely  be  ascribed  to  this  cause  only  when  it  follows  immediately  or 
shortly  after  the  known  entrance  of  a  considerable  amount  of  air  into 
the  veins. 

Animals  vary  in  their  susceptibility  to  air  embolism,  and  experi- 
mental investigation  of  the  lethal  dose  of  air  cannot  safely  be  applied 
to  man.  The  experience  of  surgeons  shows  that  the  entrance  of  a 
few  bubbles  of  air  into  a  vein  is  apparently  harmless.  The  fatal 
quantity  of  air  is  probably  at  least  several  cubic  centimeters. 

The  entrance  of  air  may  be  indicated  by  a  sound  of  suction,  pro- 
ceeding from  the  venous  opening.  Death  may  occur  almost  imme- 
diately. It  may  be  preceded  by  great  dyspnea,  cyanosis,  dilated  pupils, 
syncope  or  convulsions.    A  cardiac  murmur  may  develop.    The  pre- 

1  Reference  to  the  principal  articles  on  this  subject  may  be  found  in  Wolff's  Experi- 
mentelle  Studien  iiber  Luft  Embolie,  Virchow's  Archiv,  1903,  vol.  clxxiv. 

2  Jour,  de  Phys.,  1821,  T.  i,  p.  80.  s  jour.  Exper.  Med.,  1896,  No.  1. 


346  DISEASES  OF  THE  LUNGS. 

cordia  may  be  tympanitic  on  percussion.  The  cervical  veins  may  be 
much  dilated  and  pulsate;  the  pulse  rapid,  irregular,  and  of  small 
volume.    Most  east's  end  in  death.    Recovery  occasionally  occurs. 

The  pathologic  findings  vary  somewhat.  The  right  side  of  the  heart 
is  usually  much  dilated  and  contains  frothy  blood.  Bubbles  of  air 
are  usually  found  in  the  veins,  especially  in  those  near  the  heart, 
the  pulmonary  artery  and  its  branches.  It  is  doubtful  if  any  amount 
of  air  reaches  the  pulmonary  veins,  the  left  side  of  the  heart  and  the 
systemic  arterial  circulation  unless  through  an  open  foramen  ovale. 

Death  in  air  embolism  has  been  ascribed  to  overdistention  and 
paralysis  of  the  right  heart,  unable  to  impel  onward  a  medium  more 
compressible  than  blood.  It  has  also  been  ascribed  to  an  arrest  of  the 
air  in  the  pulmonary  capillaries,  thus  blocking  the  venous  circulation. 
This  view  is  supported  by  the  observations  of  Passet,1  Hauer,2  and 
Kose.3  In  their  experiments,  air  embolism  was  followed  by  an  increase 
of  pressure  in  the  pulmonary  artery  and  a  lowering  of  pressure  in  the 
systemic  arterial  circulation.  It  is  probable  that  pulmonary  embolism 
is  the  principal  cause.  Cardiac  embarrassment  and  cerebral  anemia 
from  a  depleted  arterial  circulation  are  probably  also  factors. 

Fat  Embolism. — The  first  observation  on  embolism  of  the  pul- 
monary capillaries  by  fat,  following  an  injury,  was  made  by  Zenker.4 
Wagner5  also  recognized  the  condition,  but  associated  it  with  suppura- 
tion and  the  formation  of  metastatic  abscesses.  Many  observations 
have  since  been  made.  Scriba's6  studies  are  especially  noteworthy. 
Fuchsig7  suggests  the  term  "traumatic  lipemia."  Connell8  has 
reviewed  the  literature. 

Pulmonary  fat  embolism  may  occur  when,  through  injury  or  dis- 
ease, liquid  fat  in  the  neighborhood  of  a  ruptured  vessel  enters  the 
systemic  venous  circulation.  It  probably  takes  place  to  some  extent 
after  all  fractures  of  bone,  but  is  more  serious  after  the  fracture  of  bones 
rich  in  fat  marrow.  Ribbert9  has  shown  that  it  may  follow  the  simple 
jarring  or  concussion  of  bone  without  fracture,  and  that  following 
fracture  it  is  often  more  extensive  than  can  be  explained  by  the  frac- 
ture alone.  It  may  occur  from  inflammation  of  and  operations  on  the 
bones,  especially  brisement  force10  and  from  trauma,  operative  injury 
or  inflammation  of  the  subcutaneous  tissue,  although  the  readiness 
with  which  venous  channels  collapse  in  such  regions  is  less  favorable 

1  Ueber  Lufteintritt  in  die  Vencn,  Arbeiten  a.  d.  Pathol.  Inst,  zu  Mi'mchen.,  1886, 
S.  293. 

2  Erscheinungen  im  grossen  und  kleincn  Kreislaufe  bci  Luftcmbolie,  Zeit.  f.  Heilk., 
1890,  vol.  xi,  S.  159. 

3  Experimentelle  Studien  uber  Lungenembolie,  Wien.  med.  Woch.,  1902,  lii,  1934, 
1989,  2038,  2091. 

4  Beitriige  z.  norm.  u.  path.  Anat.  d.  Lunge,  Dresden,  1862,  p.  31. 

*  Arch.  f.  Heilk.,  1862,  iii,  241.  e  Deut.  Zeit.-f.  Chir.,  1879,  vol.  xii. 

7  Zeit,  f.  Heilk.,  1902,  Abth.  1,  xxiii,  80. 

8  Jour.  Amer.  Med.  Assoc,  February  25,  1905. 

9  Correspondenzbl.  f.  Schw.  Aerzte.,  24,  1894,  and  Deut.  med.  Woch.,  June  28,  1900. 
10  Payr,  Zeit.  f.  Orthop.  Chir.,  1899-1900,  vol.  vii. 


THROMBOSIS,  EMBOLISM  AND  INFARCTION  347 

to  its  occurrence.  Burns  and  scalds,  contusions  and  lacerations  of  the 
liver,  the  brain,  infection  with  subsequent  fatty  degeneration  of 
organs  and  fatty  degeneration  of  thrombi  may  also  be  mentioned  as 
causes.  It  may  follow  the  subcutaneous  injection  of  oil  as  a  vehicle 
for  drugs  or  for  nutritive  purposes.1 

The  fat  lodges  in  the  smaller  branches  of  the  pulmonary  arteries  and 
the  lung  capillaries  where  it  is  recognized  on  microscopic  examination 
in  the  form  of  drops  and  cylinders  of  oil.  In  severe  cases  it  is  quite 
generally  distributed  throughout  the  lungs.  In  cases  of  exceptional 
severity,  Ribbert  estimates  that  a  half  of  all  the  capillaries  may  be 
thus  obstructed.  If  the  blocking  of  larger  vessels  tributary  to  the 
capillaries  is  taken  into  consideration,  an  exclusion  from  the  circula- 
tion of  far  more  than  half  of  the  lung  tissue  may  take  place.  In  one  of 
Ribbert's  cases,  a  clot  in  the  right  auricle  was  enveloped  in  a  thick 
layer  of  solidified  fat.  The  lungs  may  show  numerous  multiple  ecchy- 
moses.  In  some  instances  there  are  extensive  hemorrhages  and  areas 
of  pulmonary  infarction.  Pulmonary  edema  is  an  almost  constant 
postmortem  finding  in  the  human  being,  but  is  not  a  striking  feature 
in  experimental  animals,  and  is  probably  due  to  a  terminal  cardiac- 
insufficiency. 

Some  of  the  fat  passes  through  the  pulmonary  capillaries  and  is 
carried  to  other  organs,  among  which  the  brain,  the  heart,  and  the 
kidney  are  predominately  affected.  Fat  embolism  of  the  cerebral 
vessels  may  lead  to  extensive  multiple  ecchymoses  and  may  also  cause 
infarction.  Plugging  of  the  coronary  arteries  is  followed  by  patchy, 
fatty  degeneration  of  the  myocardium.  The  fat  may  be  demonstrated 
in  the  glomeruli  of  the  kidney  and  fatty  degeneration  of  the  convoluted 
tubules  may  be  found.  Welch2  suggests  that  pulmonary  fat  embolism 
may  be  of  medicolegal  importance  in  determining  whether  injuries 
have  been  inflicted  before  or  after  death. 

In  a  large  proportion  of  the  cases  in  which  fat  embolism  is  found  at 
autopsy,  it  is  merely  an  incident  in  an  otherwise  fatal  condition.  In  a 
second  and  smaller  group  of  cases  it  is  probably  a  contributing  cause 
of  death,  but  it  is  difficult  to  estimate  its  importance  in  cases  compli- 
cated by  shock,  hemorrhage  and  sepsis,  or  in  patients  with  serious 
acute  or  chronic  disease.  Finally,  cases  are  occasionally  observed 
with  extensive  fat  embolism  without  other  grave  lesions,  and  this 
condition  can  fairly  be  regarded  as  the  principal  cause  of  death.  Such 
cases  are  for  the  most  part  those  with  accidental  or  operative  injury 
of  bone,  of  itself  too  slight  to  account  for  the  fatal  termination.  In 
these  cases  it  is  not  always  easy  to  determine  whether  pulmonary, 
cerebral  or  cardiac  embolism  is  the  cause  of  death.  In  one  of  Ribbert's 
and  in  Czerny's3  case,  the  enormous  amount  of  fat  in  the  pulmonary 
circulation  seemed  an  adequate  cause.     In  the  cases  in  which  fat  is 

1  Fibiger.     Nordiskt  Medicininskt  Arkiv,  1900,  N.  F.  11. 

2  Allbutt's  System  of  Medicine,  1899,  vol.  vi. 
3Czerny,  Berl.  klin.  Woch.,  1875,  No.  44. 


348  DISEASES  OF  THE  LUNGS 

transported  through  the  lungs  to  the  brain,  fat  embolism  of  the  eerebral 
vessels  may  be  fatal.  Scriba1  regarded  this  as  the  principal  cause  of 
death.    The  cardiac  lesions  may  be  an  important  contributing  factor. 

Symptoms. — The  symptoms  which  may  be  ascribed  to  fat  embolism 
may  come  on  at  once  after  injury  or  operation.  In  such  cases, 
characteristic  symptoms  are  usually  lacking.  A  most  interesting  and 
important  feature  in  some  cases,  however,  is  an  interval  of  freedom 
from  any  symptoms  whatever.  The  patient  appears  to  be  doing 
well  and  the  indications  may  be  wholly  favorable  for  several  days 
to  a  week  or  more.  The  onset  may  be  sudden  or  gradual.  The  respi- 
rations may  then  become  rapid  and  there  is  likely  to  be  dyspnea 
which  may  be  extreme.  Pain  in  the  side,  with  or  without  the  expec- 
toration of  frothy,  blood  stained  or  hemorrhagic  sputum  may  accom- 
pany these  symptoms.  In  consequence  of  cerebral  invasion,  there  may 
be  mental  confusion,  insomnia,  delirium,  coma  or  convulsions.  In 
some  cases  there  are  paralyses  indicating  focal  lesions.  The  pulse 
is  likely  to  be  feeble,  irregular  and  rapid.  Pulmonary  and  cerebral 
symptoms  are  likely  to  be  combined.  The  temperature  is  variable. 
It  may  be  elevated,  normal  or  subnormal.  Examination  may  show 
pallor  or  cyanosis,  cold  extremities,  dilated  cervical  veins,  Cheyne- 
Stokes  respiration,  rales  suggestive  of  pulmonary  edema,  and  fat 
in  the  sputum  and  urine.  There  is  some  justification  for  the  belief 
that  cerebral  invasion  is  dependent  to  some  degree  on  the  maintenance 
of  cardiac  efficiency  and  that  the  pulmonary  type  of  the  disease  pre- 
dominates in  patients  weakened  by  disease  or  injury.  A  satisfactory 
explanation  for  the  interval  of  freedom  from  symptoms  cannot  be 
given.  The  presence  of  fat  in  the  urine  and  sputum  may  suggest  the 
diagnosis  in  doubtful  cases. 

Prognosis. — The  prognosis  of  fat  embolism  is  very  difficult  of  esti- 
mation.    It  is  of  itself  alone  probably  only  very  rarely  a  cause  of  death. 

Mercury  Embolism. — The  treatment  of  syphilis  by  the  injection 
of  insoluble  salts  of  mercury  is  occasionally  followed  not  only  by 
general  symptoms  of  poisoning,  but  by  symptoms  for  the  most  part 
or  exclusively  referred  to  the  lungs.  Various  mercury  preparations, 
such  as  the  salicylate  or  yellow  oxide  of  mercury,  gray  oil,  calomel, 
etc.,  suspended  in  liquid  petroleum,  mucilage  of  acacia,  olive  oil,  or 
other  oily  vehicle,  are  commonly  used. 

Symptoms. — When  pulmonary  symptoms  occur,  they  usually  follow 
immediately  or  soon  after  the  injection.  In  some  instances  they  are 
delayed  until  the  following  day  or  later.  The  first  indication  may  be 
a  feeling  of  thoracic  oppression  or  cough.  Expectoration  may  be  absent. 
If  present,  it  may  be  tinged  with  blood.  In  rare  instances,  the  sputum 
is  dark  red,  bloody,  and  airless.  Cyanosis,  dyspnea,  at  times  even 
orthopnea,  and  pain  resembling  that  due  to  pleurisy  are  commonly 
present.    A  chill  may  precede  the  attack.    The  temperature  is  usually 

1  Loc.  cit. 


THROMBOSIS,  EMBOLISM  AND  INFARCTION  349 

elevated.  The  pulse  may  be  rapid.  In  the  majority  of  the  cases, 
examination  of  the  lungs  is  negative.  At  times,  rales,  dulness,  bronchial 
breathing,  and  pleuritic  friction  rub  develop.  Such  signs  are  usually 
confined  to  a  circumscribed  area  in  the  posterior  and  inferior  part  of  one 
or  both  lungs. 

The  pulmonary  features  usually  predominate.  They  may  be  accom- 
panied by  general  malaise,  weakness,  insomnia,  loss  of  appetite, 
nausea  or  vomiting,  colicy  abdominal  pain,  diarrhea,  and  sweating. 
The  urine  has  occasionally  been  noted  to  be  of  high  color  and  to  con- 
tain a  trace  of  albumin. 

The  attacks  vary  much  in  intensity.  In  some  cases  the  ordinary 
occupation  has  been  followed.  More  often  in  the  reported  instances 
the  patient  has  been  confined  to  his  bed.  Neubeck1  collected  16  cases 
of  fatal  poisoning  after  the  injection  of  mercury,  adding  one  case  of 
his  own.  No  cases  with  pulmonary  symptoms  are  included  in  his 
series,  and  so  far  as  I  know,  no  fatality  from  complications  on  the  part 
of  the  lung  has  been  reported.  In  the  cases  with  pulmonary  symptoms, 
recovery  follows  at  times  in  the  course  of  a  few  hours,  usually  within 
several  days  to  a  week,  but  some  malaise  and  pallor  may  persist  for  a 
longer  time. 

No  pathologic  studies  have  been  reported  for  man,  but  the  intra- 
venous injection  of  acetic  acid  thymol-mercury  suspended  in  10  per  cent, 
liquid  petrolatum,  or  in  10  per  cent,  mucilage  of  acacia,  the  injection  of 
liquid  petrolatum,  or  10  per  cent,  watery  solution  of  mucilage  of  acacia 
alone,  in  rabbits,  was  shown  by  Moller2  to  give  rise  to  a  disturbance  of 
an  embolic  nature  in  the  pulmonary  circulation.  The  mercury  salt  in 
suspension  caused  the  most  intense  reaction  in  rabbits.  Examination 
of  the  lungs  of  animals  injected  intravenously  with  this  substance 
showed,  besides  hemorrhagic  infarction,  intense  irritation,  with  areas 
of  pneumonia  of  variable  size.  Intramuscular  injections  of  the  same 
substance  in  animals  failed  to  cause  symptoms  during  life  or  demon- 
strable changes  at  autopsy. 

The  clinical  picture  is  that  of  pulmonary  embolism,  which  probably 
arises  only  in  those  cases  in  which  the  mixture  containing  mercury 
has  been  injected  directly  into  a  vein.  In  some  of  Moller's  patients 
with  this  complication,  it  was  observed  that  the  customary  reaction 
at  the  site  of  the  injection  was  lacking. 

Statistics  vary  as  to  the  frequency  of  the  accident.  Moller3  reported 
3835  injections  in  315  patients,  observing  this  complication  43  times 
in  28  cases.  Thus  every  eleventh  patient  was  affected.  The  combined 
statistics  of  Epstein4  and  Voss5  show  22  such  complications  in  21,963 

1  Quecksilbervergiftung  mit  todlichem  Ausgange,  Dermatologische  Zeitschrift,  1902, 
vol.  ix. 

2  Ueber  Lungenembolien  bei  Injection  von  unloslichen  Quecksilberpraparaten,  Arch, 
f.  Derm.  u.  Syph.,  1896,  vol.  xxxvii. 

3  Loc.  cit. 

4  Allg.  med.  Centralzeitung,  1897,  Nos.  49  and  50,  and  Arch.  f.  Derm.  u.  Syph.,  Bd.  xl. 

5  Ueber  Hg.,  Paraffin  Embolien,  Derm.  Zeit.,  1904,  vol.  xi. 


350  DISEASES  OF   THE  LINGS 

injections  on  2281  patients;  or  one  to  every  103  cases  or  to  every  90S 
injections. 

The  danger  may  be  lessened  by  plunging  the  needle  into  the  tissue 
and  waiting  to  see  if  blood  flows  before  the  syringe  is  attached.  After 
attachment  of  the  syringe  aspiration  of  blood  should  be  attempted 
before  the  mercury  is  injected.  If  it  is  found  by  these  means  that 
the  point  of  the  instrument  lias  entered  a  vessel,  another  site  for  the 
injection  should  be  chosen.  This  is  not  always  successful  in  pre- 
venting trouble.  The  least  dangerous  site  for  the  injections  is  into 
the  muscle  in  the  upper  and  outer  gluteal  region. 

Cell  Emboli. — The  presence  within  the  pulmonary  capillaries  of 
giant  cells  from  the  bone  marrow,  liver  cells,  and  placental  (syncytial) 
giant  cells  lias  frequently  been  noted,  but  appears  to  be  of  no  special 
clinical  significance.  In  rare  instances,  masses  of  hepatic  tissue  and 
chorionic  villi  have  been  found  in  the  branches  of  the  pulmonary 
artery.  The  metastasis  of  cells  from  malignant  tumors  may  take  place 
by  way  of  the  venous  circulation  and  lead  to  secondary  deposits  in  the 
lungs. 

The  invasion  of  the  lungs  by  cells  resembling  the  megakaryocytes 
of  the  bone  marrow  is  of  special  interest.  Attention  has  been  called 
by  Foa  and  by  Verson1  to  the  prevailing  absence  of  an  intact  proto- 
plasm about  such  cells  lodged  in  the  lung.  The  nuclei  of  these  cells, 
with  or  without  a  zone  of  protoplasm  appears  to  be  practically  con- 
stant in  the  lung.  Wright2  has  noted  their  ameboid  motion,  the  pro- 
jection of  their  protoplasmic  processes  far  into  the  lumen  of  blood- 
vessels through  an  imperfect  wall  and  the  identity  in  morphology  and 
staining  reaction  of  this  cytoplasm  with  the  blood  plates.  All  grades 
of  transition  could  be  observed  between  these  bud-like  processes  and 
their  division  into  blood  plates.  It  is  probable  that  after  the  detach- 
ment of  a  part  or  the  whole  of  its  protoplasm,  the  nucleus  enters  the 
circulation  and  is  lodged  in  the  pulmonary  capillaries.  Ogata3  finds 
that  pulmonary  embolism  of  bone  marrow  tissue  may  normally  be 
observed  in  rabbits.  This  may  be  ascribed  to  concussion  of  the  bone 
marrow  and  is  more  marked  following  severe  concussion,  as  from  a  fall. 

In  his  study  of  the  histology  of  typhoid  lesions,  Mallory4  noted 
the  presence  of  large,  phagocytic,  mononuclear  cells  in  the  larger 
and  smaller  bloodvessels  and  the  capillaries  of  the  lung.  In  one  case 
of  typhoid  fever  complicated  by  typical  fibrinous  pneumonia,  he  noted 
great  numbers  of  these  cells  in  the  lung.  MacCallum5  found  extensive 
multiple  hemorrhagic  infarctions  of  the  lung  in  a  case  of  typhoid  fever. 

1  A  propos  des  transports  embolique  de  noyaux  de  megakaryocytes  dans  les  capillairs 
du  poiimon,  Arch.  ital.  de  Biologie,  1906,  vol.  xlvi. 

2  The  Origin  and  Nature  of  the  Blood  Plates,  Boston  Med.  and  Surg.  Jour.,  June  7, 
1906. 

s  Beitr.  z.  path.  Anat.  u.  z.  allg.  Path.,  1912,  liii,  120. 

4  Jour.  Exp.  Med.,  1898,  vol.  iii,  No.  6. 

5  On  the  Transportation  of  Cellular  Emboli  through  the  Thoracic  Duet  into  the 
Lungs,  Amer.  Med.,  Philadelphia,  1903,  v,  452. 


THROMBOSIS,   EMBOLISM  AND  INFARCTION  .  \'^\ 

These  were  due  to  plugging  of  branches  of  the  pulmonary  artery  with 
masses  of  cells  of  the  type  of  lymphoid  and  larger  mononuclear  phago- 
cytic cells.  These  cells  probably  reached  the  lungs  by  way  of  the 
thoracic  duct,  which  was  found  to  contain  them  in  large  masses. 

Hydatid  Embolism. — In  rare  instances,  pulmonary  embolism  may 
follow  the  detachment  or  rupture,  of  hydatid  cysts  into  the  venous 
circulation.  The  most  frequent  site  for  the  primary  growth  is  in  the 
liver  or  heart.  Gamier  and  Jomier1  collected  twelve  instances,  with 
autopsy,  from  the  literature,  and  added  one  case  of  their  own.  One 
or  more  branches  of  the  pulmonary  artery  may  be  plugged  by  the  cyst 
or  daughter  cysts.  The  sj^mptoms  do  not  differ  from  those  in  pul- 
monary embolism  from  other  causes.  The  diagnosis  may  be  suggested 
by  the  finding  of  hydatid  disease  somewhere  in  the  body. 

1  Des  embolies  hydatiques  de  l'artfere  pulmonaire,  La  Presse  medicale,  14  Juin,  1905. 


CHAPTER  XIX. 
HEMOPTYSIS. 

Expectorated  blood  may  come  from  the  mouth,  nose,  pharynx, 
esophagus,  stomach,  or  respiratory  passages.  The  term  hemoptysis 
is  usually  applied  only  to  blood  from  the  respiratory  organs  and  is 
restricted  in  the  following  discussion  to  an  origin  below  the  larynx. 

The  blood  may  consist  of  streaks  on  the  outside  of  the  sputum.    In 

other  cases  there  is  an  intimate  admixture  of  the  blood  with  the  sputum 

which  then  presents  a  pink,  red,  rusty,  purple,  or  even  black  color. 

-Pure  fluid  or  clotted  blood  may  be  expectorated.    Blood-casts  of  the 

bronchi  are  rarely  observed. 

For  convenience  of  description,  hemoptysis  may  be  classified  accord- 
ing to  the  amount  of  blood  lost  in  twenty-four  hours  as  small  (not 
exceeding  30  c.c),  moderate  (from  30  to  100  c.c),  severe  (100  to  250 
c.c),  and  profuse  (exceeding  250  c.c.).1 

Etiology. — The  causes  in  the  probable  order  of  frequency2  may  be 
enumerated  as  follows: 

1 .  Pulmonary  Tuberculosis. — This  is  probably  the  most  frequent  cause. 
The  well-known  frequency  of  pulmonary  tuberculosis  and  the  occur- 
rence of  hemoptysis  in  about  60  per  cent,  of  all  cases  during  some  part 
of  their  course  supports  this.  The  proportion  of  cases  in  which  pul- 
monary tuberculosis  occurs  as  a  cause  of  hemoptysis  differs  according 
to  the  character  and  source  of  the  material  on  which  the  statistics 
are  based.  Strieker3  estimated  that  of  900  soldiers  with  hemoptysis, 
699  (77.6  per  cent.)  were  tuberculous.  Of  909  patients  with  hemo- 
ptysis coming  to  the  Out-patient  Department  of  Brompton  Hospital, 
Jex-Blake4  regarded  497  (54.6  per  cent.)  as  tuberculous.  Of  134 
autopsy  cases  with  a  record  of  hemoptysis  in  their  past  history  or 
present  illness  at  the  Massachusetts  General  Hospital,  pulmonary 
tuberculosis  was  a  cause  in  only  14  (10  per  cent.).  The  infrequency  of 
tuberculosis  in  this  series  is  due  to  the  usual  exclusion  of  patients  with 
tuberculosis  from  the  wards  of  the  Hospital. 

2.  Pneumonia. — Lobar  pneumonia  probably  stands  next  in  frequency 
as  a  cause  of  hemoptysis.    Rusty  sputum  is  common.    Frank  hemor- 

1  Brown's  (Osier,  Mod.  Med.,  1907,  vol.  iii)  classification. 

2  I  know  of  no  trustworthy  statistics  of  the  relative  frequency  of  the  various  causes 
of  hemoptysis.    The  causes  are  here  arranged  in  the  probable  order  of  frequency. 

3  Ueber  Lungenblutung  in  der  Armee,  Festschr.  z.  100  jahrigen  Stiftungsfeier  d. 
med.-chir.  Friedrich  Wilhelm  Inst.,  Berlin,  1895. 

*  Practitioner,  1911,  lxxxvii,  616. 


HEMOPTYSIS  353 

rhage  is  rare.  Pneumonia  was  a  cause  in  42  (31  per  cent.)  of  134  cases 
of  hemoptysis  with  autopsy  at  the  Massachusetts  General  Hospital. 
In  bronchopneumonia,  blood-streaked  and  blood-tinged  sputum  may 
be  seen,  but  not  the  rusty  sputum  of  lobar  pneumonia,  and  frank 
hemorrhage  is  not  observed  in  uncomplicated  cases. 

3.  Chronic  Passive  Congestion. — The  proportion  of  cases  in  which 
this  is  concerned  apparently  falls  only  little  below  that  represented  by 
pneumonia.  The  blood  in  the  sputum  is  usually  in  bloody  streaks, 
small  bloody  masses,  or  a  frothy,  bloody  mucus.  In  some  instances 
small  blood-clots  are  expectorated.  If  the  passive  congestion  is  com- 
plicated by  pneumonia,  frank  hemorrhage  may  occur.  In  one  such 
case  two  ounces  of  blood  were  expectorated.  Cardiac  insufficiency 
is  the  common  cause  in  this  group.  Chronic  passive  congestion  was 
responsible  for  40  (29  per  cent.)  of  the  134  autopsy  cases  with  hemo- 
ptysis at  the  Massachusetts  General  Hospital.  The  section  on  Passive 
Congestion  may  also  be  consulted. 

4.  Pulmonary  Infarction. — This  is  a  much  more  common  cause  than 
is  generally  believed.  Passive  congestion  is  a  predisposing  factor 
and  is  not  infrequently  associated.  As  in  passive  congestion,  the  blood 
is  usually  in  streaks  or  masses;  at  times  clots  are  expectorated.  The 
color  may  be  bright  or  dark  red.  Frank  hemorrhage  is  rare.  Tena- 
cious, rusty  sputum  adhering  to  the  inverted  cup  and  resembling  that 
seen  in  pneumonia  may  be  observed  without  pneumonia  at  autopsy. 
Hemoptysis  from  pulmonary  infarction  may  be  an  initial  symptom 
— the  so-called  "premonitory  hemoptysis" — of  mitral  stenosis.  Stasis 
leads  to  the  formation  in  the  right  side  of  the  heart  of  thrombi,  from 
which  pieces  may  be  detached  with  resulting  pulmonary  infarction. 
Previous  symptoms  of  cardiac  disease  may  be  lacking  and  the  hemo- 
ptysis may  be  regarded  as  tuberculous  in  origin.  Infarction  was  a 
cause  of  hemoptysis  in  23  (17  per  cent.)  of  134  cases  in  this 
series. 

5.  Abscess,  Gangrene,  and  Bronchiectasis. — Blood-streaked  and  bloody 
sputum  is  more  common  than  frank  hemorrhage.  The  blood  may 
come  from  capillaries,  dilated  veins  in  the  bronchial  wall,  or  the  erosion 
of  branches  of  the  pulmonary  artery  lining  the  wall  or  traversing  the 
lumen  of  a  cavity.  Fatal  hemorrhage  may  occur.  Pulmonary  abscess 
was  a  cause  of  hemoptysis  in  3  (2  per  cent.)  of  134  cases  in  this  series 
and  bronchiectasis  in  1  (0.7  per  cent.).  Laennec1  reported  2  cases  with 
frequent  hemoptysis  during  life  and  with  bronchiectatic  cavities 
without  tuberculosis  at  autopsy.  The  bleeding  commonly  lasts  several 
days.  Fever  is  usually  absent  in  non-tuberculous  cases.  Foreign 
bodies  expectorated  from  within  may  be  a  cause  of  hemoptysis. 

6.  Aortic  Aneurysm. — This  is  among  the  less  common  causes  of  hemo- 
ptysis. Blood-streaked  or  bloody  sputum  may  come  from  the  trachea 
or  bronchi  as  a  consequence  of  pressure,  and  apart  from  any  leak  in  the 

1  Traite  de  l'auscultation  med.  et  des  mal.  des  poumons.,  Paris,  1S37,  4  ed.,  par  Andral. 
23 


354  DISEASES  OF  THE  LUNGS 

aneurysmal  sac.  Frank  hemorrhage  is  usually  due  to  the  escape  of 
blood  from  the  aneurysm,  but  is  not  always  fatal.  Osier1  refers  to  a 
patient  who  lived  for  four  years  after  a  severe  hemoptysis.  The  famous 
surgeon  Liston2  had  in  .Inly,  1S47,  a  feeling  of  constriction  at  the  top 
of  the  windpipe  and  slight  difficulty  in  swallowing.  A  profuse  hemo- 
ptysis of  thirty  to  forty  ounces  was  almost  fatal.  Although  Liston 
himself  suspected  aneurysm,  neither  Watson  nor  Forbes  could  discover 
anything  in  his  chest.  On  December  6  he  died  in  a  paroxysm  of  dyspnea. 
The  trachea  was  perforated,  but  the  opening  was  blocked  by  firm 
Laminae  of  fibrin.  Aneurysm  was  a  cause  of  hemoptysis  in  7  (5  per 
cent.)  of  134  cases  at  the  Massachusetts  General  Hospital.  In  three 
of  these  the  initial  bleeding  was  fatal. 

7.  New  Growths. — Small  amounts  of  blood  in  the  sputum  are  not 
uncommon  in  patients  with  malignant  disease  of  the  bronchi  or  lung. 
Profuse  bleeding  is  rare,  but  may  occur  in  consequence  of  the  erosion 
of  a  vessel  of  some  size.  Hemoptysis  from  malignant  disease  occurred 
in  2  cases  (1  per  cent.)  in  this  series. 

8.  Mechanical  Injuries.  —  Aspirated  foreign  bodies,  penetrating 
injuries  from  without,  a  blow  or  fall  upon  the  chest,  with  resulting 
fracture  of  the  rib,  may  be  a  cause.  Hemoptysis  following  contusion 
without  rib  fracture  is  uncommon,  and  when  it  occurs  should  lead  to 
the  suspicion  of  organic  disease,  especially  tuberculosis.  Blood  in 
the  sputum  is  occasionally  observed  in  connection  with  lung  hernia, 
and  may  be  ascribed  to  mechanical  injury  of  the  lung  at  the  hernial 
orifice.  Severe  physical  exertion  is  not  a  sufficient  cause,  and  when 
hemoptysis  follows  it  is  usually  due  to  tuberculosis.  A  strikingly 
illustrative  instance  is  found  in  the  records  of  the  Massachusetts 
General  Hospital.  In  1898  a  man,  aged  forty-six  years,  died  in  the 
hospital  of  gastric  cancer.  The  history  states  that  twenty-four  years 
before,  after  rowing  a  race,  he  coughed  up  a  lump  of  blood  as  big  as 
an  egg.  The  hemoptysis  was  not  preceded  or  followed  by  pulmonary 
symptoms.  At  autopsy  (No.  274)  the  probable  cause  of  the  bleeding 
was  found  in  obsolete  tuberculosis  of  the  lungs  and  bronchial  lymph 
glands. 

1).  Lesions  of  the  Trachea  or  Bronchi. — Ulcerative  lesions  are  usually 
a  cause  of  only  slight  hemoptysis,  but  erosion  of  a  large  vessel  may 
result  in  fatal  hemorrhage.  Syphilis  is  probably  the  most  common 
cause  in  this  group,  and  is  considered  in  the  section  on  Syphilis  of  the 
Trachea  and  Bronchi.  Tuberculous  ulceration  may  be  responsible. 
Melanotic  or  tuberculous  bronchial  lymph  glands  may  ulcerate  into 
the  air  passages  and  lead  to  erosion  of  branches  of  the  bronchial  or 
pulmonary  arteries.  Fatal  hemoptysis  may  follow.  Fibrinous  bron- 
chitis may  lead  to  hemoptysis  at  the  time  of  detachment  of  the  cast 
from  the  bronchial  wall.  In  acute  bronchitis  the  sputum  may  be 
blood-streaked  or  blood-tinged.     Hemoptysis  in  the  course  of  chronic 

1  Mod.  Med.,  vol.  iv,  p.  483.  2  Quoted  from  Osier,  ibid. 


HEMOPTYSIS  355 

bronchitis  is  usually  due  to  disturbances  in  the  lung  to  which  the 
bronchitis  is  secondary.     (See  Chronic  Bronchitis.) 

10.  Actinomycosis  is  a  rare  cause. 

11.  Leprosy. — Leprosy  according  to  Sticker1  may  be  a  cause.  Among 
142  patients  with  leprosy  seen  by  Sticker  in  India,  leprous  pulmonary 
infection  was  present  in  4,  of  whom  one  had  hemoptysis. 

12.  Constitutional  Diseases. — Hemoptysis  may  be  observed  in  dis- 
eases in  which  bleeding  occurs  elsewhere,  such  as  hemophilia, 
leukemia,  hemorrhagic  purpura,  and  scurvy. 

13.  Toxic  Causes. — Inhalation  of  irritating  fumes  from  bromin, 
chlorin,  ammonia,  and  sulphuric  acid  may  lead  to  slight  bleeding  in 
consequence  of  injury  to  the  tracheal  or  bronchial  mucous  membrane. 

14.  Animal  Parasites. — The  pulmonary  distoma  is  an  important 
cause  in  regions  where  this  parasite  prevails.  The  hepatic  distoma  is 
rarely  concerned  in  hemoptysis.  Echinococcus  disease,  filaria  san- 
guinis, and  filaria  lymphatica  may  be  mentioned  in  this  group. 

15.  Pulmonary  Aspergillosis  is  a  rare  cause. 

Other  causes  of  hemoptysis  can  for  the  most  part  be  ranged  under 
the  groups  already  discussed.  Vicarious  menstruation  is  still  occa- 
sionally mentioned,  but  there  are  no  well-authenticated  cases  in  the 
literature.  The  condition  does  not  exist  apart  from  some  pulmonary 
lesion  which  is  tuberculous  in  the  majority  of  the  cases.  There  is 
little  basis  for  belief  that  disturbances  of  the  nervous  system  (hysteria, 
epilepsy,  psychoses)  can  give  rise  to  hemoptysis.  Feigned  bleeding 
is  sometimes  encountered  in  hysterical  patients.  Sir  Andrew  Clark's2 
observations  led  him  to  believe  that  hemoptysis  at  times  occurring 
in  persons  over  fifty  was  due  to  changes  in  the  walls  of  the  pulmonary 
arteries.  Persons  of  so-called  "arthritis  diathesis"  were  affected,  and 
the  hemoptysis  was  regarded  as  of  arthritic  origin.  Betweeen  1875 
and  1889  Clark  observed  about  20  such  cases.  Today  such  cases 
might  be  found  to  belong  among  those  due  to  passive  congestion  in 
consequence  of  cardiovascular  or  renal  disease.  Similar  instances 
have  only  rarely  been  reported,  and  I  must  confess  to  scepticism  as  to 
their  classification  in  a  separate  group.  When  hemoptysis  occurs 
in  pregnancy  the  pregnancy  cannot  be  held  responsible.  Malaria 
is  not  to  be  accounted  a  cause  of  hemoptysis. 

In  emphysema,  blood-streaked  sputum  may  come  from  ruptured 
capillaries;  more  abundant  bleeding  is  probably  due  to  passive  con- 
gestion or  occurs  in  connection  with  changes  in  the  lung  to  which  the 
emphysema  is  secondary. 

Diagnosis. — It  is  at  times  difficult  to  determine  the  source  of  blood, 
whether  from  the  lungs,  mouth,  nose,  nasopharynx,  pharynx,  esophagus 
or  stomach.  If  the  blood  comes  up  with  cough  and  the  sputum  is 
blood-streaked  for  several  days  afterward  there  is  little  doubt  as  to 

1  Nothnagel's  spec.  Path.  u.  Ther.,  vol.  xiv,  Bd.  ii,  1  Abth. 

2  Remarks  on  the  Non-tubercular  and  Non-cardiac  Hemoptysis  of  Elderly  Persons, 
British  Med.  Jour.,  1889. 


356  DISEASES  OF  THE  LUNGS 

its  origin  from  the  respiratory  tract.    A  history  of  preceding  pulmonary 

disturbance  will  help  to  fix  upon  the  lungs  as  a  source.  In  recent  cases 
in  which  there  is  doubt  as  to  its  origin  the  nose,  mouth  and  naso- 
pharynx, larynx,  and  trachea  should  be  inspected.  Blood  may  flow 
from  above  downward  into  the  air  passages  and  be  expectorated  with 
cough.1 

In  some  cases  the  distinction  between  hemoptysis  and  hematemesis 
is  difficult  or  impossible.  Blood  from  the  stomach  or  esophagus  is 
usually  preceded  by  gastric  symptoms  and  expelled  by  vomiting. 
The  presence  of  food  elements  mixed  with  the  blood  may  help  in  the 
decision,  but  vomiting  may  accompany  hemoptysis  and  be  a  cause 
of  confusion  or  swallowed  blood  may  be  vomited.  Dark  chocolate- 
colored  blood  or  blood  resembling  coffee  grounds  suggests  a  gastric 
origin.  The  absence  of  blood-streaked  or  bloody  sputum  following 
the  initial  attack  may  be  of  importance.  A  history  of  tarry  stools 
or  the  persistent  presence  of  occult  blood  in  the  dejections  may  be 
helpful. 

In  difficult  cases  a  decision  that  the  lungs  are  the  source  may  be 
possible  only  after  a  most  careful  history  and  physical  examination, 
the  demonstration  of  a  pulmonary  lesion,  and  the  exclusion  of  other 
sources  of  bleeding. 

In  the  determination  of  the  cause  of  the  hemoptysis  a  distinction 
of  value  may  be  made  between  those  hemorrhages  which  occur  as  an 
initial  symptom,  or  early  in  the  course  of  an  otherwise  apparently 
mild  pulmonary  disturbance,  and  those  which  are  associated  with 
more  or  less  marked  symptoms  of  pulmonary  or  other  disease. 

In  cases  in  which  hemoptysis  occurs  out  of  a  clear  sky  or  when  cough 
and  scanty  expectoration  alone  cloud  it,  the  cause  is  almost  invariably 
pulmonary  tuberculosis.  Every  effort  should  be  made  to  obtain  evi- 
dence for  or  against  this  diagnosis  by  a  careful  history  and  as  soon  as 
it  can  safely  be  done  by  a  thorough  physical  examination.  Repeated 
and  careful  search  may  establish  this  diagnosis  by  the  finding  of  tubercle 
bacilli  in  the  sputum.  Examination  by  means  of  the  .r-rays  may  be 
helpful.  A  Wassermann  test  may  also  be  necessary.  Slight  subsequent 
fever  is  suggestive  of  a  tuberculous  origin.  Exceptions  to  the  tuber- 
culous origin  of  hemoptysis  in  this  group  are  uncommon.  Only  one 
instance,  i.  e.,  hemoptysis  from  syphilitic  ulceration  of  the  trachea, 
has  come  under  my  personal  observation.  In  rare  instances,  however, 
cases  with  premonitory  bleeding  as  a  symptom  of  latent  mitral  stenosis 
are  likely  to  be  encountered.  Unless  care  is  exercised  in  taking  the 
history  that  all  symptoms  are  included,  and  it  is  established  that  the 

1  Van  Swieten  (Commentaria  in  Hermanni  Bocrhaave,  §1198,  1773,  p.  3)  made  the 
following  interesting  observation  on  himself.  He  felt  a  slight  tickling  sensation  in  the 
fauces  and  shortly  afterward  brought  up  bloody  sputum.  This  was  followed  by  an 
irritating  cough  and  blood-tinged  expectoration.  By  means  of  a  mirror  he  recognized 
in  the  soft  palate  near  the  uvula  a  capillary  vessel  from  which  a  drop  of  blood  emerged 
about  every  two  minutes.  After  a  half-hour  the  bleeding  ceased  and  in  three  hours  the 
vessel  had  disappeared. 


HEMOPTYSIS  357 

hemoptysis  is  in  fact  an  initial  and  uncomplicated  event,  the  situation 
may  be  wrongly  interpreted.  Latent  venous  thrombosis  may,  for 
example,  lead  to  hemoptysis  from  pulmonary  embolism,  but  the 
occurrence  of  other  symptoms,  such  as  dyspnea  and  pain  in  the  side, 
may  serve  to  suggest  that  the  case  may  belong  in  the  second  group. 

When  hemoptysis  occurs  in  connection  with  more  or  less  marked 
symptoms  of  pulmonary  or  other  disease  the  causes  multiply  and  all 
enumerated  in  the  foregoing  list  are  included.,  Tuberculosis  is  here 
an  important  but  not  the  predominant  cause.  Copious  bleeding  is 
uncommon  apart  from  tuberculosis,  ruptured  aneurysm,  occasional 
cases  of  abscess  and  gangrene,  and  ulceration  of  the  trachea  and  bronchi. 
Insignificant  hemorrhage  and  prominence  of  other  symptoms  and 
signs  is  usually  seen  in  lobar  pneumonia,  chronic  passive  congestion, 
pulmonary  infarction,  abscess,  gangrene,  and  new  growths. 

Hemoptysis  in  Pulmonary  Tuberculosis. — This  may  occur  at  any  period 
of  life,  but  is  uncommon  at  the  extremes  of  age.  It  may  be  observed 
in  infancy,  as  in  the  cases  reported  by  Powell,1  Hoffnung,2  Hohlfeld,3 
Hinz,4  and  Kasten.5  In  the  cases  reported  by  Powell,  Hoffnung, 
Hinz  and  Kasten  the  bleeding  was  fatal.  Of  Strieker's  900  cases  the 
first  hemoptysis  occurred  between  the  ages  of  twenty  and  twenty-four 
in  698.  It  is  in  general  more  frequent  between  the  ages  of  fifteen 
and  thirty,  and  is  more  common  in  men  than  in  women.  Aufrecht6 
reports  fatal  bleeding  in  a  woman  aged  eighty-three. 

Hemoptysis  may  occur  in  any  pulmonary  form  of  the  disease,  but 
is  more  often  observed  in  chronic  ulcerative  tuberculosis,  of  which  it 
may  be  the  first  manifestation  or  appear  as  a  symptom  at  any  part  of 
its  course.  It  appears  to  be  more  common  in  the  earlier  stages  of  the 
chronic  ulcerative  type  and  a  higher  blood  pressure  at  this  period  has 
been  suggested  as  a  cause,  but  this  is  doubtful.  In  the  majority  of  cases 
the  bleeding  occurs  during  ordinary  activity,  and  is  not  infrequent 
in  the  early  morning  hours  when  the  patient  is  abed.  In  a  small 
proportion  of  cases  hemoptysis  follows  some  unusual  physical  exertion, 
mechanical  injury,  such  as  a  blow  or  fall,  excitement,  or  exposure  to 
cold.  In  some  instances  an  acute  exacerbation  of  the  tuberculous 
process  precedes  the  hemoptysis.  In  women  recurrent  hemoptysis 
may  be  observed  at  the  time  of  the  catamenia.  Hemoptysis  may 
follow  the  removal  of  pleural  effusion  as  in  one  of  my  cases. 

Patients  who  have  once  had  hemoptysis  are  very  likely  to  have  it 
again  and  numerous  attacks  are  not  uncommon.  In  some  instances 
the  sputum  may  be  constantly  blood-stained  over  a  period  of  months 
or  years. 

1  British  Med.  Jour.,  May  30,  1874. 

2  Ueber  Hamoptoe  bei  Kindern.,  Inaug.  Diss.,  Berlin,  1885. 

3  Monatsschr.  f.  Kinderheilk,  1903. 

4  Ueber  profuse  Hamoptoe  im  fruhen  Kindesalter  bei  der  Lungentub.,  Inaug.  Diss., 
Leipzig,  1903. 

5  Zur  Lehre  der  Hamoptoe  im  Sauglingsalter,  Beitr.  z.  Klinik  d.  Tub.,  1906,  v,  431 

6  Path.  u.  Ther.  d.  Lungenschwindsucht,  1913,  2  Auf.,  p.  203. 


358  DISEASES  OF  THE  LUNGS 

Pathology.  -Blood-streaked,  pink,  red,  or  rusty  sputum  may  come 
from  capillaries  in  a  congested  bronchial  mucosa  or  the  pulmonary 
tissue  by  a  process  of  diapedesis.  Larger  amounts  of  blood  usually 
have  their  origin  in  rupture  of  an  aneurysmal  dilatation  of  a  branch 
of  the  pulmonary  artery,  lining  the  wall  or  traversing  the  lumen  of  a 
pulmonary  cavity.  According  to  Kidd's1  observations,  aneurysmal 
dilatation  of  the  vessel  lying  within  a  cavity  is  common  and  consists 
of  a  lateral  expansion  of  the  vessel  on  its  exposed  side.  In  rare  instances 
an  artery  traversing  the  lumen  of  the  cavity  may  be  uniformly  dilated 
to  form  a  fusiform  aneurysm.  The  aneurysms  vary  in  size  from  a  pin's 
head  to  a  plum,  but  seldom  exceed  the  size  of  a  cherry.  They  are 
usually  single,  but  may  be  multiple,  and  in  one  case  Kidd  found  22 
in  one  lung.  Rupture  of  the  sac  is  the  most  frequent  cause  of  profuse 
hemoptysis.  In  a  series  of  80  cases  of  fatal  bleeding  a  ruptured 
aneurysm  was  found  in  70.  In  a  small  proportion  of  cases  erosion 
and  ulceration  of  the  wall  of  the  vessel  within  a  cavity,  without  the 
formation  of  aneurysm,  may  be  responsible  for  the  bleeding.  At  times 
a  main  branch  of  the  pulmonary  artery  may  be  involved,  but  usually 
the  bleeding  comes  from  a  medium-sized  branch.  In  one  instance 
West'-  found  ulceration  of  a  branch  of  the  pulmonary  vein  as  a  cause 
of  fatal  bleeding. 

Symptoms. — In  tuberculous  cases  in  which  bloody  sputum  is  expec- 
torated there  are  usually  no  other  special  symptoms.  When  pure  blood 
is  suddenly  expectorated  the  patient  may  be  conscious  during  a  cough- 
ing spell  of  a  tickling  sensation  in  the  throat  and  then  of  a  warm  fluid 
with  a  salty  taste  in  the  mouth.  Cough  may  be  absent.  Following  the 
attack  more  blood  is  usually  brought  up  on  coughing  or  clearing  the 
throat,  and  the  sputum  is  commonly  bloody  for  several  days  after  the 
attack.  In  some  cases  the  patient  is  wakened  from  sleep  by  the  attack. 
He  may  be  uncertain  of  the  origin  of  the  blood,  and  respiratory  symptoms 
suggesting  the  lungs  as  a  source  may  be  absent,  but  this  is  uncommon. 
Slight  fever  is  usually  present  for  several  days  after  the  hemoptysis 
(Fig.  47),  and  may  be  due  to  absorption  of  aspirated  blood,  but  is 
more  often  a  consequence  of  extension  of  the  tuberculous  process  by 
the  aspiration  of  infected  blood.  The  amount  of  blood  lost  is  usually 
small  and  without  appreciable  affect  on  the  course  of  the  underlying 
tuberculous  process. 

If  the  hemorrhage  is  large,  the  blood  may  pour  from  the  mouth 
and  nostrils.  Nausea  and  vomiting  may  accompany  the  attack  and 
swallowed  blood  may  be  vomited.  Anxiety  and  restlessness  are  likely 
to  follow7  an  initial  or  profuse  hemoptysis.  Acceleration  of  the  pulse, 
elevation  of  the  rate  of  respiration,  and  dyspnea  may  be  observed  in 
the  more  severe  cases.  A  repetition  of  the  bleeding  is  likely  to  follow 
on  successive  days  or  at  longer  or  shorter  intervals.  Sufficient  blood 
may  be  lost  in  one  attack  to  exsanguinate  the  patient  or  profuse 

1  Allbutt  and  Rolleston's  System  of  Medicine,  vol.  v,  p.  320. 

2  Diseases  of  the  Organs  of  Respiration,  1902,  i,  384. 


HEMOPTYSIS 
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Hemoptysis  in  an  afebrile  patient.  Subsequent  elevation  of  temperature  and  persis- 
tence until  death  six  weeks  later.  Fatal  termination  due  to  rapid  extension  of  the 
tuberculous  process  probably  as  a  consequence  of  the  hemorrhage.      (V.  Z.;  C.  H.) 


360  DISEASES  OF  THE  LUNGS 

bleeding  may  recur,  as  in  West's1  case,  in  which  on  the  average  a 
half-pint  of  blood  was  expectorated  daily  for  forty-five  days.  In  the 
last  attack  thirty-seven  ounces  were  brought  up  and  the  patient  died 
of  suffocation.  Death  may  take  place  suddenly  from  suffocation, 
cerebral  anemia,  and  syncope,  after  an  interval  from  exhaustion,  or  by 
rapid  extension  of  the  tuberculous  process  in  the  lung.  The  aspiration 
of  infected  blood  into  nearby  or  remote  regions  is  likely  to  increase 
the  extent  of  the  pulmonary  involvement.  Tuberculous  broncho- 
pneumonia is  the  most  common  result  of  such  aspiration,  but  acute 
miliary  tuberculosis  or  acute  pneumonic  phthisis  may  occur.  Dyspnea, 
rapid  pulse,  high  fever,  cyanosis  and  death  may  follow  the  more 
extensive  invasions. 

Physical  signs  on  examination  of  the  chest  are  usually  those  of  the 
underlying  disease.  If  the  hemoptysis  occurs  at  an  early  stage  of  the 
tuberculous  process  the  examination  may  be  negative.  In  some  cases 
rales  limited  to  the  involved  region  or  distributed  over  a  wider  area 
may  be  heard.  They  may  be  due  to  blood  in  the  branches  of  the 
bronchi.  At  the  time  of  the  bleeding,  physical  examination,  if 
attempted  at  all,  should  be  cursory  and  limited  to  auscultation  of  the 
breath  sounds,  the  voice  and  whisper  and  testing  the  tactile  fremitus. 
Percussion  should  be  avoided  and  the  patient  should  not  be  allowed 
to  attempt  forced  breathing. 

Prognosis. — This  is  difficult  to  estimate  and  depends  on  many 
factors.  There  are  cases  in  which  hemoptysis  as  an  initial  symptom  or 
early  in  the  course  of  an  apparently  mild  respiratory  disturbance  is 
the  first  intimation  of  the  tuberculous  nature  of  the  disease  and  leads 
to  a  more  immediate  decision  on  adequate  measures  for  relief.  In 
such  instances,  success  in  securing  an  arrest  of  the  tuberculous  process 
may  be  largely  dependent  on  this  timely  warning.  But  in  the  majority 
of  cases,  hemoptysis  appears  to  influence  the  outlook  little  if  at  all. 
Brown2  finds,  however,  in  an  analysis  of  1810  cases  from  the  records 
of  the  Adirondack  Cottage  Sanitarium  that  males  with  hemoptysis 
did  not  do  as  well  during  sanitarium  residence  as  those  without  hemop- 
tysis, and  that  of  1276  cases  discharged  from  the  institution  two  to 
twenty  years  previously  a  slightly  larger  number  of  deaths  occurred 
among  those  who  had  hemoptysis.  In  females  a  similar  result  was  not 
shown. 

Outspoken  tuberculosis  does  not  necessarily  follow  hemoptysis, 
which  may  occur  in  patients  with  apparent  good  health  and  sound 
lungs.  Of  329  instances  of  hemoptysis  observed  by  Ware,3  62  (18  per 
cent.)  recovered  without  subsequent  symptoms  to  suggest  pulmonary 
tuberculosis.  The  interval  elapsing  between  the  attack  of  hemoptysis 
and  the  last  report  was  over  ten  years  in  41  cases.  In  1768  Goethe,4 
at  the  age  of  nineteen  and  then  a  student  at  Leipsig,  had  an  attack 

1  Loc.  cit.,  p.  388.  2  Osier.     Mod.  Med.,  1907,  iii,  280. 

3  Hemoptysis  as  a  Symptom,  1860. 

4  Aus  meinem  Leben.,  Dichtung  und  Wahrheit,  2  Th.,  p.  300. 


HEMOPTYSIS  361 

as  follows:  "One  night  I  waked  with  a  severe  hemoptysis  and  had 
enough  strength  and  presence  of  mind  to  wake  my  room-mate.  .  .  . 
For  several  days  I  wavered  between  life  and  death."  For  some  months 
he  thought  he  had  pulmonary  tuberculosis  and  must  die  young.  At 
the  age  of  eighty-two  he  had  hemoptysis  again  and  died  at  the  age  of 
eighty-three.  His  long  and  active  life  may  serve  as  a  comforting 
example  to  those  who  need  encouragement.  At  the  age  of  twenty- 
three  or  twenty-four,  Rousseau1  expectorated  blood  and  gave  up  his 
work  as  a  teacher  of  singing.    He  died  at  the  age  of  sixty-six. 

Hemoptysis  per  se  is  rarely  fatal.  Winsch2  observed  fatal  bleeding 
only  twice  among  100  patients  with  hemoptysis.  Death  as  the  imme- 
diate result  of  bleeding  occurred  in  only  1  of  76  patients  with  hemo- 
ptysis at  the  Channing  Home  and  2  of  142  patients  at  the  Massa- 
chusetts General  Hospital.  Death  as  a  consequence  of  extension  of 
pulmonary  infection  for  which  the  hemorrhage  was  probably  in  part 
responsible,  occurred  in  1  other  case  (See  Chart,  Fig.  48)  at  the 
Channing  Home  and  6  other  cases  at  the  Massachusetts  General 
Hospital. 

Treatment. — Blood-streaked  or  blood-tinged  sputum  is  an  indication 
for  cessation  of  all  exertion  for  a  few  days. 

More  abundant  bleeding  is  an  indication  for  the  immediate  adoption 
of  such  measures  as  tend  to  favor  thrombosis  at  the  point  of  rupture 
of  the  bleeding  vessel  and  cessation  of  the  hemorrhage.  The  chief 
danger  is  not  that  the  hemoptysis  will  prove  fatal  from  loss  of  blood, 
but  that  the  tuberculous  process  will  be  extended  into  previously 
unaffected  parts  of  the  lung  by  the  aspiration  of  infected  blood.  The 
excitement  and  anxiety  attendant  on  the  bleeding  increase  this  danger 
by  increasing  the  depth  of  respiration  and  inducing  the  patient  to 
yield  to  unnecessary  inclination  to  cough.  It  is  first  necessary  to  calm 
the  fears  of  the  patient  and  the  family.  Reassuring  examples  of 
recovery  are  not  far  to  seek  and  can  be  drawn  from  every  physician's 
experience.  In  a  very  large  proportion  of  the  cases  the  hemorrhage 
ceases  spontaneously  and  careful  nursing  is  all  that  is  required. 

The  patient  should  be  put  to  bed  and  kept  absolutely  quiet  in  a 
semi-recumbent  position,  cautioned  not  to  speak  unnecessarily,  and 
then  not  above  a  whisper.  Unproductive  cough  should,  so  far  as  pos- 
sible, be  suppressed.  The  patient  should  not  be  allowed  to  feed  him- 
self, and  urine  and  stool  should  be  passed  into  the  urinal  or  bed-pan. 
The  diet  should  be  light  and  easily  digestible.  All  food  may  well  be 
withheld  for  a  few  hours  after  the  bleeding.  Fluids  should  be  restricted 
to  from  one  to  one  and  a  half  quarts  a  day  and  given  in  small  portions 
at  a  time  to  avoid  overfilling  of  the  bloodvessels.  If  the  hemorrhage 
is  severe,  the  amount  of  fluid  should  still  further  be  restricted  and  the 
quantity  of  food  limited  for  several  days.    Food  should  be  given  either 

1  Confessions,  i,  Livre  5. . 

2  Beitrage  z.  Kenntniss  der  Hamoptoe  phthisicorum,  Diss.,  Berlin,  1898,  quoted  from 
Sticker,  Nothnagel's  spec.  Path.  u.  Ther.,  xiv,  Bd.  ii,  1  Abt. 


362  DISEASES  OF  THE  LUNGS 

cold  or  warm,  and  not  hot.  Tea,  coffee,  and  alcohol  should  not  be 
allowed.  Acids  may  prolong  coagulation  time  and  should  not  be  given. 
If  the  bowels  fail  to  move  an  enema  is  to  be  preferred  to  cathartics. 
Increased  intrathoracic  pressure  from  straining  at  stool  may  dislodge 
an  occluding  thrombus  and  renew  the  hemorrhage. 

The  room  should  be  well  ventilated  and  cool,  hut  chilling  of  the 
patient's  body  is  to  be  avoided.  Visitors  should  be  excluded  and  the 
utmost  quiet  and  serenity  should  prevail.  Only  a  cursory  physical 
examination  should  be  made  at  the  time  of  the  hemorrhage  and  a 
thorough  examination  postponed  until  at  least  two  weeks  after  the 
bleeding  has  ceased.  The  patient  should  be  absolutely  at  rest  in  bed 
as  long  as  there  is  fever  and  for  at  least  a  week  after  cessation  of  the 
hemoptysis.  Tuberculin  should  not  be  used  for  diagnostic  purposes 
until  at  least  a  month  has  elapsed.  Only  urgent  reasons  justify  the 
removal  of  pleural  fluid  during  or  soon  after  hemoptysis. 

The  use  of  opium  is  a  common  practice  in  the  treatment  of  hemop- 
tysis, but  it  has  both  disadvantages  and  advantages.  Cough  is 
necessary  for  the  expectoration  of  blood  in  many  cases,  and  to  prevent 
cough  may  only  increase  the  danger  of  retention  of  infected  material 
within  the  air  passages.  On  the  other  hand,  expulsive  efforts  with 
cough  may  dislodge  a  partially  adherent  thrombus  and  maintain  or 
renew  the  hemorrhage.  Morphine  gr.  f  (0.008  gm.)  or  codein  gr.  \ 
(0.016  gm.)  may  be  used  to  quiet  irritative  and  unproductive  cough 
or  extreme  nervousness,  but  should  not  be  used  as  a  routine. 

Of  other  measures,  an  ice-bag  over  the  heart  may  be  quieting. 
Pieces  of  ice  in  the  mouth  and  salt  on  the  tongue  are  popular  remedies, 
and  if  not  of  value,  are  at  least  probably  not  harmful.  Too  much  ice 
by  mouth  may  unduly  increase  the  volume  of  body  fluid. 

Of  the  following  measures,  none  have  been  shown  to  have  any 
definite  effect  in  controlling  the  hemorrhage.  Of  the  so-called  hemo- 
statics, gallic  acid  gr.  10  (0.650  gm.),  tannic  acid  gr.  10  (0.650  gm.), 
mineral  acids,  especially  dilute  sulphuric  acid,  HI  10  (0.60  c.c),  alum 
gr.  10  (0.650  gm.),  the  perchloride  of  iron,  Tr.  ferri  perchloridi  TTL  10 
(0.60  c.c),  acetate  of  lead  gr.  2  (0.130  gm.),  and  the  fluid  extract  of 
ergot  dram  1  (4  c.c.)  are  sometimes  used.  Calcium  lactate  may  be 
given  in  doses  of  gr.  15  (0.975  gm.)  three  times  a  day  for  three  days 
and  then  omitted  for  two  days.  Astringent  inhalations,  such  as  the 
vapor  of  turpentine  (a  teaspoonful  of  the  oil  on  a  handkerchief  placed 
in  front  of  the  mouth),  or  tannic  acid,  or  alum  gr.  10  to  20  (0.650  to 
1.300  gm.)  to  the  ounce  in  the  form  of  a  spray  are  probably  valueless. 

Theoretical  considerations  have  led  to  the  use  of  emetics,  such  as 
tartar  emetic  gr.  \  to  \  (0.0162  to  0.032  gm.)  every  hour  till  nausea 
and  vomiting  is  produced,  ipecacuanha  gr.  1  to  2  (0.065  to  0.130  gm.) 
every  quarter  to  half  hour,  or  apomorphin  hydrochlorate  gr.  -^V  to 
Y$  (0.0032  to  0.0043  gm.)  subcutaneously.  Their  purpose  was  to 
convert  partial  into  complete  rupture  of  the  injured  vessel  in  order  that 
the  severed  ends  might  retract  and  thus  favor  cessation  of  the  bleeding. 


HEMOPTYSIS  363 

Dislodgement  of  an  occluding  thrombus  and  fresh  hemorrhage  is  more 
likely  to  follow  than  any  favorable  action,  and  they  should  no1  be  used. 
Reduction  of  blood-pressure  in  the  pulmonary  circuit  by  the  use  of 
sodium  nitrate  gr.  2  to  5  (0.130  to  0.325  gm.),  amy]  nitrite  (3  to  5 
drops  in  a  glass  perle)  and  nitroglycerin  gr.  , •/,„  (0.00065  gm.)  presents 
theoretical  advantage,  but  there  is  no  evidence  that  diminution  of 
pulmonary  pressure  takes  place.  Pituitary  extract  and  atropin  sul- 
phate gr.  T^-$  (0.00065  gm.)  have  also  been  recommended.  Con- 
striction of  the  pulmonary  vessels  by  means  of  the  subcutaneous  use 
of  adrenalin  is  purely  hypothetical,  and  if  systemic  blood-pressure 
were  raised,  might  aggravate  the  hemorrhage. 

Venesection  was  formerly  a  common  practice  for  the  purpose  of 
lowering  blood-pressure,  stopping  the  pulmonary  hemorrhage  and 
preventing  death  from  suffocation,  but  is  now  universally  abandoned. 
A  similar  purpose  is  the  basis  of  treatment  by  constriction  of  the 
extremities  by  an  elastic  ligature.  The  two  thighs  just  above  the  knee, 
the  two  upper  arms  or  all  four  extremities  are  so  far  constricted  as  to 
obstruct  the  return  venous  flow,  without  obliteration  of  the  pulse, 
thus  withholding  blood  in  the  extremities.  The  obstruction  may  be 
maintained  on  three  limbs  at  a  time  and  then  gradually  released, 
each  limb  in  rotation,  one  ligature  being  changed  every  twenty  minutes. 
This  may  be  considered  as  a  life-saving  measure  in  the  presence  of 
profuse  hemorrhage. 

The  subcutaneous  injection  of  gelatin  cannot  be  recommended. 
The  use  of  fresh  animal  (rabbit)  serum  is  said  to  control  hemorrhage 
by  increasing  coagulation.  Thirty  cubic  centimeters  may  be  used 
subcutaneously.  In  one  case  of  persistent  hemoptysis  in  which  I 
used  it,  no  effect  was  obtained. 

Limitation  of  motion  of  the  affected  side  by  application  of  the  ice- 
bag,  a  sand-bag,  the  lateral  decubitus,  adhesive  plaster  or  artificial 
pneumothorax  has  been  recommended.  Inasmuch  as  the  tuberculous 
process  is  bilateral  in  a  very  large  proportion  of  the  cases,  it  is  usually 
impossible  to  tell  from  which  side  the  bleeding  comes,  and  the  immo- 
bilization of  the  unaffected  side  may  throw  an  additional  burden  on 
the  other  and  aggravate  the  bleeding.  While  successful  limitation 
of  motion  of  the  affected  side  may  favor  the  cessation  of  hemorrhage, 
it  may  prevent  the  expulsion  of  blood  and  thus  increase  the  danger 
of  infection.  To  judge  from  my  cases,  the  hemorrhage  itself  is  less 
menacing  to  life  than  spread  of  the  infection  by  the  effused  blood. 
Artificial  pneumothorax  is  more  dangerous  than  hemorrhage.  Attempts 
at  immobilization  may  do  more  harm  than  good. 

In  the  presence  of  an  hemoptysis  so  profuse  as  to  seem  likely  to  be 
immediately  fatal,  the  use  of  intravenous  normal  saline  solution  may 
be  considered.  In  one  case  (No.  136,772)  after  a  very  abundant 
hemoptysis,  the  patient  became  unconscious,  the  pulse  very  weak 
and  irregular,  and  the  extremities  cold.  Consciousness  returned  after 
a  saline  infusion  had  been  given,  but  the  patient  died  within  a  few 
hours  from  a  recurrence  of  the  bleeding. 


CHAPTER  XX. 
PULMONARY  SYPHILIS. 

Many  of  the  older  writers  speak  of  phthisis  due  to  lues.  Little  atten- 
tion was  paid  to  the  condition,  however,  until  Depaul1  in  France, 
and  Yirchow2  in  Germany,  published  more  accurate  anatomic 
studies.  In  spite  of  many  recorded  cases  and  of  careful  anatomic 
and  histologic  studies,  there  is  still  little  agreement  concerning  the 
features  of  the  disease.  Syphilis  only  rarely  affects  the  lungs.  The 
diagnosis  cannot  be  made  with  assurance  during  life,  and  is  often 
uncertain  at  the  postmortem.  The  chief  difficulty  lies  in  the  exclusion 
of  other  diseases,  especially  tuberculosis,  which  may  produce  a  similar 
picture.  The  literature  to  1882  is  collected  by  Hiller3  and  from  1879  to 
1899  by  Flockemann.4    The  literature  is  also  reviewed  by  Herxheimer.5 

Two  clinical  types  of  the  disease  are  recognized:  the  hereditary  and 
the  acquired  forms. 

1.  Hereditary  Form. — As  a  result  of  congenital  syphilis,  there  may 
be  circumscribed  pulmonary  lesions  or  gummata  and  a  diffuse  invasion 
of  the  pulmonary  tissue  or  'pneumonia.  The  two  lesions  are  frequently 
combined.  They  are  usually  associated  with  other  manifestations  of 
congenital  syphilis,  such  as  coryza,  various  syphilides,  enlargement 
of  the  liver  and  spleen,  and  emaciation.  If  the  infant  lives,  the  respira- 
tory involvement  may  be  evidenced  by  cyanosis  and  dyspnea,  but 
physical  examination  of  the  chest  is  practically  always  negative. 

The  pregnancy  rarely  proceeds  to  full  term,  and  depending  on  the 
extent  of  the  pulmonary  and  other  lesions,  the  infant  is  stillborn  or 
lives  only  a  few  hours  or  days.  In  very  rare  instances,  there  may  be 
late   manifestations   of   pulmonary   syphilis. 

(a)  Gummata. — These  are  rare  manifestations  of  congenital  syphilis. 
They  consist  of  circumscribed  interstitial  changes  with  some  tendency 
to  necrosis  and  cavity  formation.  Pulmonary  gummata  in  the  new- 
born have  been  described  by  Martineau,6  Chiari,7  Schinze,8  Kokawa,9 
and  others.  The  process  does  not  differ  from  similar  changes  found 
in  the  acquired  form  with  which  it  will  be  described. 

(b)  Pneumonia. — In  this  group  may  be  included  Virchow's  white 
pneumonia,  with  which  interstitial  changes  are  often  combined,  or 

1  Soc.  anatom.,  1837.  2  Virchow's  Arch.,  1847,  vol.  i. 

3  Charite  Armalen.,  1882,  ix,  184. 

4  Zentralb.  f.  allg.  Path.,  Bd.  x,  pp.  469  and  964. 

6  Ergeb.  d.  allg.  Path.  u.  path.  Anat.,  Lubarsch  u.  Ostertag,  1906,  II. 

6  Soc.  anat.,  1862.  7  Wien.  med.  Presse,  1895,  p.  349. 

8  Beitr.  zur  congenit.  Lungensyph.  Inaug.,  Diss.,  Leipzig,  1902. 

9  Arch.  f.  Dermat.  u.  Syph.,  1906,  vol.  lxxviii. 


PULMONARY  SYPHILIS  365 

occur  as  a  late  stage  of  the  more  active  process.  Of  the  various  pul- 
monary manifestations  of  syphilis,  white  pneumonia  is  the  best  estab- 
lished type.  It  is  chiefly  of  anatomic  interest,-  since  the  diagnosis 
of  the  condition  cannot  be  made  during  life  and  the  infants  are  still- 
born or  die  soon  after  birth.  One  instance  (Autopsy  2892)  of  congenital 
syphilitic  pneumonia  was  found  among  3000  autopsies  at  the  Massa- 
chusetts General  Hospital. 

Parts  or  the  whole  of  one  or  both  lungs  may  be  involved.  The 
affected  lung  is  enlarged  and  firm  and  may  show  the  impressions  of 
the  ribs.  The  external  and  cut  surface  is  dry  and  pale,  yellowish, 
grayish  or  reddish-white  in  color,  and  may  have  a  marbled  appearance. 
Excised  pieces  sink  in  water.  The  cut  surface  has  the  appearance  of 
white  hepatization,  but  is  more  often  smooth  and  without  the  granular 
appearance  found  in  ordinary  pneumonia.  The  condition  has  been 
called  "  pancreatization"  from  the  resemblance  to  the  cut  surface  of 
the  pancreas.  The  pleura  is  usually  free.  The  subpleural  tissue  may 
be  thickened,  vascular,   and  infiltrated. 

On  microscopic  examination,  both  parenchymatous  and  interstitial 
changes  are  usually  found.  Cases  in  which  the  alveolar  epithelium 
is  desquamated,  swollen  and  has  undergone  fatty  degeneration  repre- 
sent the  parenchymatous  form  or  true  pneumonia  alba  of  Virchow. 
Cases  with  proliferation  of  the  interstitial  tissue  alone  without  changes 
in  the  parenchymatous  tissue  are  classed  as  interstitial  pneumonia. 
Such  a  distinction  between  the  two  forms  is  maintained  by  Hiller,1 
Heller,2  Stroebe,3  Spanudis,4  Frankel,5  and  others.  In  most  of  the 
reported  cases,  however,  changes  in  the  parenchymatous  and  interstitial 
tissue  have  been  associated,  and  it  is  questionable  whether  a  sharp 
distinction  between  the  two  groups  is  justified.  Heubner,6  Birsch- 
Hirschfeld,7  Ziegler,8  Orth,9  Schinze,10  and  Kokawa11  believe  that  there 
is  only  one  form  of  pneumonia.  This  is  white  pneumonia  in  its  broader 
sense,  and  changes  in  the  parenchyma  and  interstitial  changes  are 
combined.  According  to  Kokawa,  the  interstitial  changes  are  the 
more  constant,  being  present  in  all  of  four  cases  which  he  studied, 
while  the  involvement  of  the  epithelium  was  variable. 

The  interstitial  tissue  is  increased  in  amount  by  proliferation  of  the 
fixed  connective-tissue  cells  and  infiltration  with  small  mononuclear 
and  occasionally  with  polynuclear  cells.  The  interstitial  changes  vary 
in  different  cases  and  in  different  parts  of  sections  from  the  same  case. 

1  Charite-Annalen.,  1882,  ix,  184. 

2  Deut.  Arch.  f.  klin.  Med.,  1884,  xlii,  159. 

3  Zentralb.  f.  allg.  Path.  u.  path.  Anat.,  Bd.  ii,  p.  1009. 

4  Ueber  kongenitale  Lungensyph.,  Freiburg,  1891,  Inaug.,  Diss. 

6  Spez.  Path.  u.  Ther.  der  Lungenkrankheiten,  1904. 

R  Gerhardt's  Handbuch  der  Kinderkrankheiten,  1896. 

7  Lehrbuch  der  path.  Anat.,  1894. 

8  Lehrbuch  der  allg.  Path.  u.  path.  Anat.,  1902,  Bd.  ii. 

9  Lehrb.  der  Spez.  path.  Anat.,  1887,  p.  447. 

10  Beitrag  zur  Kong.,  Lungensyph.,  Leipzig,  1902,  Inaug.  Diss. 

11  Archiv  f.  Dermat.  u.  Syph.,  1906,  vol.  Ixxviii. 


366  DISEASES   OF   THE   LUNGS 

Its  increase  may  be  noted  in  the  interalveolar  septa,  but  is  especially 

marked  about  the  bronchi  and  the  bloodvessels. 

The  alveoli  and  smaller  bronchi  are  wholly  or  partially  filled  with 
desquamated  epithelial  cells,  leukocytes,  and  red  blood  corpuscles. 
The  desquamated  epithelium  may  be  swollen,  fatty  or  necrotic.  The 
alveolar  walls  may  be  thickened. 

The  capillary  bloodvessels  are  widened.  The  walls  of  the  larger 
vessels  are  thickened.  The  adventitia  is  most  affected,  is  infiltrated 
and  vascular.  Interstitial  changes  have  been  observed  in  the  media. 
In  rare  instances  thickening  of  the  intima  has  been  noted.  From  the 
observation  of  most  advanced  changes  in  the  perivascular  tissue,  it 
has  been  thought  that  this  represents  the  starting-point  of  the  process. 

The  lymph  spaces  may  be  widened.  Kokawa  has  noted  that  the 
elastic  fibers  are  less  developed  in  the  lungs  of  the  fetus  with  syphilitic 
pneumonia  than  in  normal  lungs  at  a  corresponding  age.  The  pleura 
may  be  thickened  or  unchanged. 

The  spirochseta  pallida  has  been  found  in  the  pulmonary  tissue  by 
Levaditi,1  Beriel  and  Favre,2  Jambon,3  and  others.  The  organism 
is  more  abundant  in  the  diseased  tissue  than  elsewhere,  but  may  also 
be  found  in  the  blood  and  in  non-specific  lesions  in  infected  infants. 

Relation  of  Congenital  Pulmonary  Syphilis  and  Tuberculosis. — It  is 
stated  that  the  two  lesions  may  be  combined  in  the  same  lung,  and 
although  this  may  be  true,  owing  to  the  difficulty  of  differentiating 
syphilis  and  tuberculosis,  proof  of  the  syphilitic  character  of  such 
combined  lesions  is  thus  far  wanting.  Infants  with  undoubted  con- 
genital syphilis  in  extrapulmonary  regions  may  have  pulmonary  tuber- 
culosis, and  tubercle  bacilli  may  be  found  in  the  lesions  at  the  post- 
mortem examination.  Caseous  syphilitic  pneumonia  has  been  described 
but  is  not  substantiated. 

2.  Acquired  Form. — The  pulmonary  manifestations  of  acquired 
syphilis  are  rare.  Fowler4  could  find  only  twelve  specimens  believed 
to  illustrate  syphilitic  lesions  in  the  lungs  in  the  museums  of  the  London 
Hospitals  and  the  Royal  College  of  Surgeons.  Of  these,  two  were 
doubtful.  Osier5  states  that  among  2500  autopsies  at  the  Johns 
Hopkins  Hospital,  there  were  twelve  cases  in  which  lesions  ascribed 
to  syphilis  were  found.  Among  3000  autopsies  at  the  Massachusetts 
General  Hospital,  one  case  (Autopsy  29)  with  syphilitic  ulceration 
of  the  trachea  and  indurative  pneumonia  with  cavity  formation  was 
found.    The  syphilitic  character  of  the  pulmonary  lesions  is  doubtful. 

Bronchial  catarrh  may  be  an  early  manifestation  of  the  secondary 
period  of  syphilis,  corresponding  to  the  cutaneous  eruption  of  the  same 
period.  Gummata  of  the  trachea  and  bronchi  may  occur  as  a  late 
secondary  or  tertiary  manifestation.    Tracheal  and  bronchial  stenosis 

1  Annates  dc  L'Institut  Pasteur,  January,  1900. 

-  Soc.  med.  des  hop.,  Lyon,  1906.  3  Th.  de  Lyon,  July,  1900,  p.  134. 

4  The  Diseases  of  the  Lungs,  Fowler  and  Godlee,  1898,  p.  429. 

6  Osier.    Modern  Medicine,  vol.  iii,  p.  471. 


P  ULMONA  It  Y  S  Y PHI  US 


367 


is  not  uncommon  as  a  result  of  the  contraction  of  the  sear  tissue. 
Pulmonary  gummata  and  interstitial  changes  are  usually  late  manifes- 
tations of  acquired  syphilis  and  occur  during  the  tertiary  period.  They 
seldom  appear  until  two  years  have  elapsed,  but  may  be  found  after 
eighteen  to  twenty  years. 

Pathology. — (1)  Gummata. — These  may  be  single  or  multiple,  and 
vary  in  size  from  a  hemp  seed  to  a  walnut.  They  may  be  found  in  any 
part  of  the  lung,  but  are  more  commonly  within  than  on  the  surface. 
They  show  a  special  disposition  to  develop  at  the  root  of  the  lung, 
but  may  at  times  be  found  in  the  lower  lobes;  least  often  at  the  apices. 
Diffuse  fibroid  induration  is  often  associated  with  gumma. 

In  its  early  stages,  a  gumma  is  said  to  be  soft,  yellowish  in  color, 
irregular  in  shape  and  surrounded  by  pale  red  or  grayish  tissue.  Later, 
it  may  be  reddish,  yellow,  gray  or  white.  Fatty  degeneration  and 
connective-tissue  formation  take  place.  Caseation  may  occur.  Inflam- 
mation in  the  neighboring  tissue  may  lead  to  the  formation  of  a  capsule. 
Necrosis  with  evacuation  into  the  bronchi  may  result  in  cavity  for- 
mation, but  this  is  rare.  Finally,  tough  connective-tissue  scars  of  a 
white,  gray  or  even  black  color,  from  the  deposit  of  pigment,  may  be 
found.  If  at  the  periphery  of  the  lung,  these  may  lead  to  indentation 
or  puckering  of  the  pleura.  Calcareous  masses  may  arise  from  the 
deposition  of  lime  salts. 

Fig.  49 


Spirochtette  in  lung  tissue.      (Koch.) 


On  microscopic  examination,  proliferation  of  the  connective-tissue 
cells  about  the  bloodvessels,  the  bronchi  or  in  the  interlobular  tissue 
is  found.  Necrosis  may  prevent  the  recognition  of  individual  elements 
of  the  tissue.  Connective-tissue  outgrowths  may  proceed  from  the 
mass  into  the  surrounding  tissue.    The  adjacent  alveoli  and  alveolar 


368  DISEASES  OF  THE  LUNGS 

walls  contain  an  excess  of  proliferated  epithelial  cells.  The  histologic 
picture  in  gumma  does  not  differ  essentially  from  that  in  syphilitic 
interstitial  pneumonia.  The  bloodvessels  play  an  important  part 
in  the  process.  They  may  be  thrombosed  and  their  walls  may  be 
thickened. 

The  spirocrueta  pallida  is  difficult  of  demonstration  in  the  syphilitic 
lesions  of  the  lung  as  in  similar  lesions  of  other  organs.  It  has  been 
found  in  acquired  syphilitic  pulmonary  lesions  by  Koch1  and  Schmorl.2 
The  spirochseta  pallida  must  be  carefully  differentiated  from  non- 
syphilitic  spirochsetse,  which  may  be  present  in  the  lung  tissue. 

2.  Diffu.se  Fibroid  Induration. — Interstitial  changes  of  variable 
extent  may  occur  independently  of  gummata  or  in  association  with 
them.  The  connective-tissue  may  spring  from  the  perivascular,  the 
peribronchial  or  the  subpleural  connective  tissue.  Parts  or  the  whole 
of  one  lung  may  be  involved.  The  changes  are  common  at  the  hilus. 
Bronchiectasis  frequently  accompanies  the  fibrosis.  Caseation  is 
uncommon,  and  tubercle  bacilli  are  absent.  The  microscopic  picture 
is  not  distinctive  of  syphilis.  It  is  to  be  remembered  that  in  cases  in 
which  tracheobronchial  syphilis  is  present,  bronchostenosis  may  give 
rise  to  inflammatory  and  indurative  changes  in  the  pulmonary  terri- 
tory supplied  by  the  stenotic  bronchi,  and  that  the  virus  of  syphilis 
may  not  be  immediately  concerned  in  the  pulmonary  process. 

3.  Bronchopneumonia. — It  is  doubtful  whether  this  can  be  ascribed 
to  syphilis. 

Symptoms. — There  are  no  symptoms  distinctive  of  pulmonary 
syphilis.  Gummatous  lesions  alone  are  usually  without  symptoms. 
Even  quite  extensive  interstitial  pneumonia  may  fail  to  give  rise  to 
symptoms.  When  these  occur,  they  are  usually  due  to  an  accom- 
panying bronchiectasis.  Cough  and  dyspnea  may  be  prominent 
features,  their  intensity  varying  with  the  extent  of  the  lesions.  The 
sputum  presents  nothing  characteristic.  It  may  be  abundant,  and 
purulent  and  at  times  is  offensive.  Hemoptysis  may  occur  from  the 
erosion  of  arteries  lining  the  walls  or  traversing  the  lumen  of  pulmonary 
cavities.  It  is  less  common  than  in  tuberculosis.  Pain  may  be  present, 
but  is  not  a  prominent  feature  from  the  infrequency  with  which  the 
pleura  is  affected.  Night  sweats  may  occur.  Emaciation  may  exist 
with  extensive  pulmonary  disease.  In  the  early  stages  the  disease 
is  afebrile,  but  hectic  fever  may  be  present  later  in  its  course. 

Physical  Signs. — Uncomplicated  gummata  usually  fail  to  give  rise 
to  physical  signs.  With  extensive  interstitial  pneumonia  and  bron- 
chiectasis, the  signs  are  such  as  may  be  present  in  similar  processes 
from  other  causes.  A  location  of  pulmonary  changes  elsewhere  than 
at  the  apices  may  be  suggestive. 

Diagnosis. — 1.  Clinical. — In  the  newborn  the  diagnosis  cannot  be 
made.     The  possibility  of  pulmonary  syphilis  in  children  who  have 

1  Verhandl.  d.  dent.  path.  Gesellsch.,  1907,  p.  275.  2  Ibid. 


PULMONARY  SYPHILIS  369 

suffered  from  hereditary  syphilis  should  be  borne  in  mind.  The 
association  of  pulmonary  symptoms  with  interstitial  keratitis,  Hutch- 
inson's "notched  teeth,"  labial  fissures,  nasal  and  palatal  ulceration, 
depression  of  the  bridge  of  the  nose,  tibial  and  cranial  nodes  and  deaf- 
ness may  be  suggestive.  In  the  acquired  form  of  the  disease,  the 
symptoms  and  signs  will  usually  suggest  pulmonary  tuberculosis. 
The  diagnosis  cannot  be  made  with  certainty,  but  the  following  con- 
siderations may  serve  to  suggest  that  the  case  is  one  of  pulmonary 
syphilis  and  not  tuberculosis,  (a)  Undoubted  evidence  of  syphilitic- 
infection,  followed  by  secondary  manifestations  and  the  coexistence 
with  the  pulmonary  process  of  other  tertiary  syphilitic  lesions.  Ulcera- 
tion or  stenosis  of  the  trachea  or  bronchi  is  especially  suggestive. 
(b)  Absence  of  family  history  or  opportunities  for  contagion  of  tuber- 
culosis, (c)  Positive  Wassermann  test,  (d)  The  absence  of  tubercle 
bacilli  from  the  sputum  in  repeated  examinations,  (e)  Negative 
subcutaneous  tuberculin  injections  in  increasing  doses  up  to  and 
including  10  mg.  (/)  A  pulmonary  lesion  outside  the  apices  of  the 
lungs,  as  determined  by  physical  examination  or  the  .r-rays.  Syphilitic- 
processes  are  most  often  at  the  root  or  at  the  bases  of  the  lungs,  (g) 
Improvement  of  the  pulmonary  symptoms  under  antisyphilitic  treat- 
ment. Little  can  be  expected  from  this  in  an  advanced  stage  of  the 
disease. 

2.  Pathologic. — It  cannot  be  said  as  yet  that  even  at  autopsy 
the  syphilitic  character  of  pulmonary  lesions  can  be  conclusively 
established. 

In  the  distinction  between  congenital  syphilitic  and  croupous 
pneumonia  in  the  newborn,  the  histologic  picture  may  be  suggestive. 
Less  abundant  fibrin,  less  marked  interstitial  and  vascular  changes 
and  involvement  of  the  pleura  are  more  characteristic  of  lobar  pneu- 
monia, while  the  presence  of  extrapulmonary  signs  of  congenital 
syphilis  and  the  discovery  of  the  spirochseta  pallida  in  properly  stained 
sections  of  the  lung  tissue  speak  for  syphilitic  pneumonia.  Pulmonary 
tuberculosis  must  also  be  excluded. 

In  the  diagnosis  of  congenital  or  acquired  gummatous  or  interstitial 
pulmonary  processes,  the  following  points  must  be  considered,  (a) 
The  previously  mentioned  clinical  features  (a  to  e  above)  may  furnish 
important  evidence.  (6)  Caseation,  necrosis,  cavity  formation  and 
pulmonary  aneurysms  are  more  characteristic  of  tuberculosis  than  of 
syphilis,  (c)  When  pulmonary  cavities  occur  in  syphilis,  they  are 
more  likely  to  be  bronchiectatic  in  origin,  (d)  Changes  in  the  blood- 
vessels are  more  common  in  syphilis.  Giant  cells  are  more  often  seen 
in  tuberculosis,  (e)  Demonstration  of  spirochseta  pallida  in  the  lesions. 
(/)  Finally,  the  careful  search  for  tubercle  bacilli  in  stained  sections 
and  the  inoculation  of  a  guinea-pig  with  a  piece  of  the  suspected  tissue 
must  be  negative. 

Fibroid  changes  with  or  without  bronchiectasis  may  follow  pul- 
monary suppuration  from  other  causes  than  syphilis  and  tuberculosis. 
24 


370  DISEASES  OF   THE  LUNGS 

The  cause  of  such  changes  may  be  sufficiently  obvious  from  the  history 
of  the  case.  Neither  on  gross  nor  histologic  examination  can  they 
be  positively  differentiated  from  interstitial  changes  due  to  syphilis. 
In  such  cases,  reliance  must  be  placed  on  the  distribution  of  the  lesions 
and  the  presence  of  associated  syphilis  with  other  factors  in  any  given 
instance. 

Prognosis. — This  depends  largely  on  the  extent  of  syphilitic  invasion 
of  the  lungs  and  other  organs  and  on  the  early  recognition  of  the 
disease.  The  complete  recovery  from  pulmonary  lesions,  the  syphilitic 
character  of  which  is  highly  probable,  has  repeatedly  been  observed 
under  antisyphilitic  treatment.  When  the  pulmonary  disease  has 
progressed  to  extensive  fibroid  changes  and  bronchiectasis,  the  prospects 
for  recovery  are  hopeless,  but  some  alleviation  may  be  expected. 

Treatment. — General  measures  similar  to  those  for  pulmonary  tuber- 
culosis should  be  instituted.  These  consist  in  rest,  extra  feeding  and 
fresh  air.  Mercury  and  salvarsan  are  chiefly  to  be  relied  upon  in 
syphilis  of  the  lung  as  in  syphilis  of  other  organs.  The  earlier  the 
treatment  is  begun,  the  better  the  results  which  may  be  expected. 
Alternating  courses  of  the  protiodid  of  mercury  and  of  salvarsan  intra- 
venously are  most  efficient.  Treatment  should  be  controlled  by  the 
Wassermann  test. 


CHAPTER  XXL 
PULMONARY  ACTINOMYCOSIS. 

Etiology. — Bollinger1  first  showed  that  the  disease  of  cattle  pre- 
viously known  as  a  form  of  sarcoma  of  the  jaw  was  due  to  a  vegetable 
parasite  to  which  Llarz2  gave  the  name  of  "Actinomyces  bovis"  because 
of  its  radiate  structure.  Soon  afterward,  J.  Israel3  discovered  the 
parasite  in  man.  He  includes  in  his  publication  an  observation, 
making  it  apparent  that  the  organism  had  been  seen  as  early  as  1845 
by  v.  Langenbeck.4  The  identity  of  the  human  and  bovine  infections 
was  first  pointed  out  by  Ponfick.5 

The  first  extensive  studies  on  the  biology  of  the  organism  were 
made  by  Bostroem6  and  by  Wolff  and  Israel.7  Their  widely  different 
views  are  responsible  for  much  of  the  confusion  which  has  since 
obtained.  It  is  now  known  that  Bostroem  and  many  subsequent 
investigators,  beginning  their  experiments  with  material  containing 
true  Actinomyces,  have  in  many  instances  cultivated  therefrom  a 
group  of  contaminating  organisms  properly  classed  among  the 
Streptothrices.  This  confusing  group  is  widely  distributed  in  nature, 
being  found  not  only  as  an  occasional  cause  of  suppurative  lesions 
in  man  and  cattle,  but  also  on  grains  and  grasses.  Wolff  and  Israel, 
on  the  other  hand,  undoubtedly  worked  with  true  actinomyces.  Their 
investigations  have  been  confirmed  by  many  investigators,  notably 
by  Wright,8  whose  painstaking  research  has  finally  placed  the  biology 
of  actinomyces  upon  a  firm  foundation. 

Actinomyces  Bovis. — No  difference  has  been  established  between  the 
organism  found  in  man  and  in  animals.  It  is  present  in  the  lesions  and 
in  the  pus  in  the  form  of  spherical  or  irregularly  rounded,  grayish  or 
yellowish  granules,  varying  in  size  from  minute  particles  to  a  diameter 

1  Cent,  f.  d.  med.  Wissensch.,  1877,  p.  481.  2  Ibid.,  p.  484. 

3  Virchow's  Arch.,  1878,  Ixxiv,  15. 

4  Hermann  Lebert  (Traite  d'anat.  path.  gen.  et  spec,  2  vol.  Text  in  Fol.  8,  2  vol. 
Atlas  in  Fol.,  Paris,  1857-61,  i,  54.  Atlas,  vol.  i,  cl.  ii,  Fig.  16)  speaks  of  "Corps  par- 
ticuliers  trouve  dans  le  pus"  and  describes  them.  His  figures  show  that  they  were 
actinomyces.  The  descriptions  given  by  Rivolta  (Sarcoma  fibroso  al  bordo  inferiore 
della  brancha  mascellare  sinistra  del  bove,  Medico  veterinario,  January,  1868,  p.  125). 
Robin  (Traite  de  microscopie,  Paris,  1871,  p.  576,  Fig.  157),  and  Perroncito  (Osteo- 
sarcoma della  mascella  anteriore  e  posteriore  nel  bovini.  Article  Pathologia  dell' 
Enciclopedia  agraria  italiana,  diretta  dal  Dottore  Gaetano  Cantani,  1875,  iii,  599), 
show  that  the  organism  had  also  been  seen  by  them. 

6  Berl.  klin.  Woch.,  1879,  No.  23,  p.  345. 

6  Beitr.  z.  path.  Anat.  u.  z.  allg.  Path.,  1890. 

7  Virchow's  Arch.,  1891,  cxxvi,  11.  8  Jour.  Med.  Research,  May,  1905. 


372 


DISEASES  OF  THE  LUNGS 


of  1  to  2  mm.    These  may  be  soft,  tallowy  and  easily  crushed  or  hard, 
resistant  and  even  calcified.     By  the  aggregation  of  small  colonies 


Fig.  50 


> 


/> 


%■ 


o      ski 


-O 


.-•- 


Actinomyces  granule.      (J.  Israel.) 
Fig.  51 


;0^*"~-. 


L«*S«gS 


t&?$Mi 


Crushed  actinomyces  granule  from  fresh  sputum.     Unstained.      X  750. 

a  mulberry-shaped  mass  may  be  produced.    In  mucopurulent  sputum, 
the  granules  may  be  found  entangled  in  the  mucus.     In  fluid  pus, 


PULMONARY  ACTINOMYCOSIS  373 

they  may  gravitate  to  the  bottom  of  the  reeeptacle.  They  are  more 
easily  recognized  if  the  specimen  of  sputum  is  poured  into  a  glass  dish 
containing  water  amounting  to  several  times  the  volume  of  sputum. 
In  this  the  more  coherent  masses  of  sputum  may  be  teased  apart 
by  means  of  the  platinum  wire.  The  granules  tend  to  sink  to  the  bot- 
tom.   Examination  on  a  black  background  will  facilitate  the  search. 

When  crushed  between  slide  and  cover  glass,  typical  granules  appear 
under  the  low  power  of  the  microscope  as  yellowish  granular  masses, 
relatively  transparent  in  the  central  parts  and  with  a  narrow,  denser, 
irregular  margin.  Under  the  high  power,  an  indefinite  mass  of  tangled 
fibers,  debris  and  pus  cells  are  found  at  the  centre  and  at  the  per- 
iphery a  dense  network  of  interlacing  filaments.  At  the  extreme 
margin,  are  isolated  branching  filaments  and  radiating,  hyaline,  and 
refractive  club-shaped  bodies,  thickest  at  or  near  the  distal  extremity. 
The  "clubs"  or  rays  are  the  distinctive  feature  of  the  granules.  They 
are  not  always  present,  but  in  their  absence  the  colonies  cannot  be 
identified  with  certainty  in  fresh  specimens.  In  the  report  of  cases 
as  actinomycosis  of  the  lung,  a  failure  to  record  the  fact  that  the 
granules  are  club-bearing  may  suggest  the  possibility  of  confusion 
with  particles  composed  of  streptothrix  filaments.  Club  formation 
is  probably  a  means  of  protection  against  the  destructive  action  of 
the  tissue  cells  and  fluids. 

Smears  may  be  made  from  the  crushed  granules  and  stained  by 
Gram's  method.  After  decolorization  with  alcohol,  the  specimen  is 
washed  in  water,  stained  for  a  few  seconds  with  a  saturated  aqueous 
solution  of  eosin,  again  washed,  cleared  with  absolute  alcohol  and  with 
xylol  and  mounted  in  balsam.  The  filaments  then  appear  as  Gram- 
staining  slender-branched  and  unbranched  wavy  threads.  Thicker 
filaments  are  occasionally  seen.  At  times  they  increase  in  size  toward 
one  end,  forming  a  slender  club.  These  are  not  the  true  clubs,  but 
appear  to  be  simple  variations  in  the  morphology  of  the  organism. 
A  striking  feature  of  some  of  the  filaments  is  the  presence  of  deeply 
staining  points,  giving  them  a  beaded  appearance.  The  true  clubs 
are  stained  with  eosin  and  can  be  readily  recognized.  Their  number 
in  stained  smears  made  from  the  granules  is  usually  less  than  in  fresh 
specimens  from  the  same  material,  suggesting  that  the  clubs  are  washed 
away  or  dissolved  in  the  process  of  staining.  Their  radial  position 
at  the  periphery  of  the  colony  is  also  likely  to  be  disturbed  by  the 
manipulations. 

The  organism  may  be  isolated  by  the  following  method,  employed 
by  Wright:1  Granules  should  first  be  thoroughly  washed  in  sterile 
salt  solution  or  bouillon,  then  crushed  and  disintegrated  between  two 
sterile  glass  slides.  Only  such  masses  as  show  an  abundance  of  fila- 
ments should  be  chosen  for  cultivation.  The  disintegrated  granule 
is  transferred  by  means  of  a  platinum  loop  to  several  test-tubes  con- 

1  Jour.  Med.  Research,  May,  1905. 


374 


DISEASES  OF  THE  LUNGS 


taining  1  per  cent,  dextrose  agar  to  a  depth  of  about  7  to  8  cm.  and 
cooled  to  about  40°  C.    An  even  distribution  of  the  material  through- 


Fig.  52 


Gross  appearance  of  sugar-agar  suspension  cultures  of  actinomyces. 
(Dr.  J.  H.  Wright.) 

Fig.  53 


A  colony  of  actinomyces  in  a  section  of  sugar-agar  suspension  culture. 
(Dr.  J.  H.  Wright.) 


out  the  agar  is  accomplished  by  means  of  the  loop  and  the  tube 
placed  in  the  incubator.     At  the  same  time  a  number  of  granules 


PULMONARY  ACTINOMYCOSIS 


/><» 


should  be  placed  on  the  sides  of  sterile  test-tubes  plugged  with  cotton 
and  kept  at  room  temperature  in  the  dark.  If  there  is  little  or  no 
contamination  of  the  material  with  other  organisms,  the  colonies 
of  actinomyces  may  be  expected  to  develop  within  a  few  days  to  a 
week.  A  small  portion  of  the  agar  containing  colonies  is  removed, 
placed  on  a  clean  slide  and  examined  under  the  low  power  of  the  micro- 
scope. By  this  means,  a  small  section  of  the  agar  containing  a  single 
colony  may  be  separated  from  the  mass,  thoroughly  washed  of  adherent 

Fig.  54 


Colony  of  actinomyces  with  well-developed  "clubs"  at  the  periphery  in  a  nodule 
in  the  peritoneal  cavity  of  a  guinea-pig  inoculated  with  a  culture  of  the  organism. 
(Dr.  J.  H.  Wright.) 


bacteria  in  sterile  bouillon,  again  transferred  to  melted  agar  and  placed 
in  the  incubator.  If  many  colonies  of  contaminating  bacteria  are 
present,  isolation  will  probably  be  impossible  by  this  means.  An 
attempt  may  then  be  made  to  isolate  the  organism  from  the  granules 
dried  on  the  sides  of  the  sterile  tubes,  in  which  it  may  be  expected  that 
a  large  number  of  the  contaminating  bacteria  have  been  killed  after 
a  period  of  two  to  three  weeks. 

Actinomyces  are  anaerobic  and  grow  well  only  in  agar  or  bouillon. 


376  DISEASES  OF  THE  LUNGS 

In  1  per  cent,  dextrose  or  glucose  agar  suspension  cultures  after  two  to 
four  days  in  the  incubator,  the  growth  is  most  abundant  in  a  narrow 
zone  from  5  to  10  mm.  below  the  surface,  while  scattered  colonies 
appear  throughout  the  medium  below.  Colonies  in  cultures  are  in 
general  similar  to  those  in  the  lesions  of  the  disease,  and  are  composed 
of  spherical  masses  of  interlacing  and  branching  filaments  disposed 
in  a  more  or  less  radiate  manner.  The  growth  in  bouillon  usually 
occurs  in  the  form  of  whitish,  coherent,  spherical  masses  at  the  bottom 
of  the  tube,  without  surface  growth  or  the  production  of  cloudiness 
in  the  medium.  In  the  other  usual  culture  media  and  at  room  tem- 
perature, little  or  no  growth  takes  place.  Spore  formation  is  not 
observed.  Wright  succeeded  in  reproducing  the  club-formation,  so 
characteristic  of  the  colonies  in  tissues,  by  growing  actinomyces  in 
such  animal  fluid  as  blood-serum  and  serous  pleuritic  fluid.  The 
organism  withstands  drying  at  room  temperature  for  fifty  to  eighty 
days. 

The  attempt  to  reproduce  the  disease  experimentally  in  animals  has 
failed  to  give  rise  to  a  progressive  lesion  comparable  to  the  disease 
in  man  and  cattle.  The  results  of  intraperitoneal  inoculation  of  guinea- 
pigs  and  rabbits  with  bouillon  cultures  are  inconstant.  In  some  instances 
small  connective-tissue  nodules  containing  one  or  more  cavities  filled 
with  pus  are  produced  in  or  upon  the  omentum.  These  lesions  in 
their  anatomic  and  histologic  appearance  are  identical  with  typical 
actinomycosis,  but  little  evidence  is  thus  obtained  that  the  organism 
has  multiplied  within  the  animal  body. 

The  practically  constant  occurrence  of  mixed  infection  with  various 
bacteria  in  spontaneous  actinomycotic  lesions  and  the  failure  to 
produce  a  progressive  infection  in  animals  after  inoculation  with  pure 
cultures  suggest  that  contaminating  bacteria  play  an  important  part 
in  the  disease.  In  explanation  of  the  rare  instances  of  spontaneous 
infection  with  actinomyces  alone,  an  increased  individual  suscepti- 
bility may  be  assumed. 

Mode  of  Infection. — The  prevalent  view  that  infection  takes  place 
through  the  inhalation  of  dust  or  local  injury  from  dried  grains  or 
grasses  is  based  on  the  assumption  that  the  disease  is  due  to  organisms 
of  the  type  described  by  Bostroem.  The  organisms  of  this  group  grow 
well  on  all  culture  media  at  room  temperature  and  in  the  incubator. 
They  grow  even  on  sterilized  water  and  can  be  demonstrated  on  grains 
and  grasses.  They  have  not  been  shown,  however,  to  cause  lesions 
like  actinomycosis  after  experimental  inoculation  of  animals. 

There  is  no  conclusive  evidence  that  actinomycosis  is  contagious. 
Growth  of  true  actinomyces  in  artificial  media  occurs  only  at  about 
37°  C.  and  it  is  therefore  unlikely  that  multiplication  of  the  organism 
takes  place  under  any  ordinary  conditions  outside  the  human  or  animal 
body.  Wright  suggests  that  it  is  a  normal  inhabitant  of  the  alimentary 
canal,  gaining  entrance  to  the  tissues  as  do  other  bacteria  through 
local  wounds  or  abrasions.     Foreign   bodies  have  occasionally  been 


PULMONARY  ACTINOMYCOSIS  2>11 

found  within  lung  tissue  the  site  of  actinomycosis.  In  Balack's1  case, 
a  barley-grain  was  found  in  a  pulmonary  cavity.  Israel2  found  a 
fragment  of  a  carious  tooth  at  autopsy  in  an  abscess  cavity  of  the  left 
upper  lobe.  It  is  probable  that  actinomyces,  as  well  as  other  organisms, 
may  thus  at  times  be  implanted  in  the  lung. 

Fig.  55 


M 


Actinomycosis  of  the  omentum  in  a  guinea-pig  forty-five  days  after  intraperitoneal 
inoculation  with  material  from  the  tonsillar  crypts  of  a  patient  without  actinomycosis. 
X  750. 

That  infection  with  actinomycetes  arises  from  within  the  individual 
from  organisms  present  in  the  buccal  cavity  is  supported  by  my  experi- 
ments.3 The  intraperitoneal  inoculation  of  guinea-pigs  with  the  con- 
tents of  carious  teeth  and  the  tonsillar  crypts  from  persons  free  from 
actinomycosis  gave  rise  to  omental  tumors  histologically  identical 
with  actinomycotic  tissue  and  containing  typical  club-bearing  actino- 
myces granules.  In  order  to  completely  establish  the  identity  of  these 
organisms  with  actinomyces  bovis,  pure  cultures  should  be  obtained, 
and  with  such  cultures  it  should  be  possible  to  produce  in  animals 
lesions  similar  to  those  obtained  with  pure  cultures  of  actinomyces 
isolated  from  human  or  bovine  actinomycosis.  Attempts  to  isolate 
the  organism  in  pure  culture  by  various  means  have  thus  far  failed. 
Its  isolation  from  material  obtained  from  the  teeth  and  the  tonsils 

1  Ueber  Lungen-Aktinomykose,  Inaug.  Diss.,  Leipzig,  1893. 

2  Arch.  f.  klin.  Chir.,  Bd.  xxxiv,  p.  160. 

3  Lord,  Jour.  Amer.  Med.  Assoc,  1910,  lv,  1261. 


378  DISEASES  OF  THE  LUNGS 

and  from  the  experimental  lesions  in  animals  is  rendered  especially 
difficult  by  the  abundance  of  the  contaminating  bacteria.  From 
these  considerations,  until  proof  is  offered  to  the  contrary,  actinomy- 
cosis may  be  regarded  with  probability  as  arising  from  organisms 

harbored  in  and  about  the  teeth  and  in  the  crypts  of  the  tonsils. 

Occupation  appears  to  have  no  bearing  on  the  development  of  pul- 
monary actinomycosis.  Both  sexes  are  about  equally  affected.  The 
disease  occurs  most  frequently  between  twenty  and  forty  years  of  age. 

Pathogenesis. — Infection  of  the  lung  may  occur  as  a  primary  affec- 
tion or  secondary  to  the  disease  in  neighboring  or  remote  organs. 

Primary  Pulmonary  Actinomycosis. — The  disease  is  most  frequent  in 
the  region  of  the  head  and  neck.  Infection  of  the  lung  or  abdomen 
stands  next  in  frequency.  Of  105  cases  collected  by  Rutimeyer,1  the 
lungs  were  involved  in  22  (20  per  cent.).  Of  the  421  cases  reported 
by  Illich,2  the  lung  was  primarily  affected  in  58  (13.7  per  cent.).  The 
manner  in  which  the  organism  gains  entrance  to  the  lung  is  uncertain. 
Aspiration  from  the  buccal  or  pharyngeal  cavity  is  a  possible  source. 

Secondary  Pulmonary  Actinomycosis. — This  is  much  less  common. 
The  disease  may  arise  by  extension  from  neighboring  organs.  Infection 
about  the  jaws  or  neck  may  descend  along  the  prevertebral  region 
to  the  mediastinum,  and  thence  invade  the  lung.  Extension  may 
likewise  occur  from  the  esophagus  or  through  the  diaphragm  from 
the  abdomen.  A  subdiaphragmatic,  hepatic,  perinephritic  or  peri- 
typhlitic  abscess  may  be  the  starting  point  of  the  disease.  Infection 
of  the  pleural  sac  may  be  prevented  if  an  adhesive  pleurisy  precedes 
the  rupture.  In  a  considerable  proportion  of  all  cases  of  actinomycosis, 
whether  of  the  lung  or  other  organs,  metastatic  distribution  of  the 
organism  occurs  in  the  later  stages  of  the  process.  Invasion  of  blood- 
vessels may  follow  the  softening  of  infected  tissue  and  erosion  of  the 
vessel  wall.  The  detachment  of  an  infected  thrombus  thus  formed 
may  carry  the  organism  into  remote  parts  of  the  body  by  way  of  the 
arterial  or  venous  circuit,  the  latter  being  most  common.  Rupture 
into  the  portal  system  results  in  secondary  involvement  of  the  liver, 
while  invasion  of  the  systemic  veins  leads  to  secondary  deposits  in 
the  lung.  Israel3  noted  metastatic  distribution  of  actinomyces  in 
one  of  his  cases  and  many  similar  observations  have  since  been  made. 
In  a  few  instances,  the  portal  of  entry  into  the  circulation  has  been 
found.  Thus  Ponfick4  found  a  mass  projecting  into  the  lumen  of  the 
jugular  vein,  and  regarded  this  as  the  source  of  a  soft  tumor  the  size 
of  an  apple,  containing  actinomyces  granules,  in  the  right  auricle. 
Hanau5  noted  perforation  into  the  superior  vena  cava  in  a  case  of 
actinomycosis  of  the  left  lung  and  pericardium.    Benda6  has  reported 

1  Berl.  klin.  Woch.,  1889,  Nos.  3  and  4. 

2  Beitrag.  z.  Klinik.  d.  Aktinomykose,  Wien,  1892. 

3  Virchow's  Arch.,  1878,  vol.  lxxiv. 

4  Ueber  Actinomykose,  Berl.  klin.  Woch.,  1880,  No.  46,  p.  660. 

0  Zwei  Fiille  von  Actinomycose  Correspondenzbl.  f.  Schw.  Aerzto,  1889,  xix,  165. 
c  Zwei  Fiille  von  metastat.  Aktinomykose,  Deut.  med.  Woch.,  1900,  No.  13. 


PULMONARY  ACTINOMYCOSIS  370 

a  case  of  actinomycosis  of  the  liver  leading  to  perforation  of  an  hepal  ic 
vein,  with  secondary  actinomycotic  thrombosis  of  the  inferior  vena 
cava  and  death  from  pyemia.  In  a  second  case,  actinomycosis  of  the 
heart  wall  and  actinomycotic  thrombi  in  a  coronary  vein  were  found. 

Dissemination  by  way  of  the  lymph  channels  occurs  only  in  rare 
instances  if  at  all.  Slight  inflammatory  hyperplasia  of  the  bronchial 
glands  is  common.  Histologic  examination,  however,  usually  fails 
to  show  lesions  characteristic  of  the  disease  or  filaments  which  can  with 
certainty  be  regarded  as  actinomyces.  In  Balack's1  case,  on  the  other 
hand,  a  gland  at  the  tracheal  bifurcation  was  enlarged  to  the  size  of 
a  pigeon's  egg  and  contained  actinomyces  granules  within  small  areas. 

Pathology. — Changes  in  the  pulmonary  tissue  as  a  result  of  invasion 
by  actinomyces  closely  resemble  the  lesions  in  chronic  ulcerative 
pulmonary  tuberculosis.  Connective-tissue  formation  is  more  abun- 
dant, however;  sinuous  and  communicating  tracts  are  more  common, 
and  extension  to  neighboring  organs  and  the  thoracic  wall  is  more 
often  observed. 

The  gross  appearance  of  the  lung  presents  a  variable  and  usually 
complicated  picture.  The  more  characteristic  lesions  comprise  areas 
of  bronchopneumonia  and  interstitial  pneumonia,  multiple  abscesses 
and  bronchiectasis.  Bronchitis  is  almost  invariably  present.  Lobar 
pneumonia,  gangrene  and  tuberculosis  occur  as  complications  in  rare 
instances.  Pulmonary  tuberculosis  and  actinomycosis  were  associated 
in  Hebel's2  and  in  one  of  the  Massachusetts  General  Hospital  cases 
(Autopsy  1488). 

There  is  no  pathologic  evidence  in  favor  of  a  purely  bronchial  form, 
but  the  terminations  of  the  bronchi  are  almost  invariably  implicated 
in  the  process,  and  the  infection  spreads  by  extension  and  the  aspira- 
tion of  organisms  into  neighboring  or  remote  parts  of  the  lungs.  The 
lower  lobes  are  principally  affected,  the  left  somewhat  more  commonly 
than  the  right.  The  disease  is  usually  unilateral.  In  Schlagenhaufer's3 
case,  there  was  diffuse  involvement  of  both  lungs  in  the  form  of  puru- 
lent bronchitis,  peribronchitis,  multiple  bronchiectasis  and  broncho- 
pneumonia and  indurative  pneumonia,  with  consecutive  interstitial 
and  vesicular  emphysema.  Primary  invasion  of  the  upper  lobes  has 
been  noted,  as  in  9  of  the  58  cases  collected  by  Illich,4  in  3  of  which  the 
apices  were  involved.  Lindt's5  case  is  noteworthy  because  of  the  find- 
ing at  autopsy  of  actinomycotic  cavities  at  the  apices  of  both  lungs. 
Other  instances  of  apical  localization  have  since  been  reported. 

In  its  early  stages  the  disease  appears  as  scattered  or  circumscribed, 
isolated,  grayish,  yellowish  or  reddish-brown,  resistant  pulmonary 
areas,  which  on  section  are  found  to  contain  pus,  the  evacuation  of 
which  discloses  cavities  lined  with  grayish-yellow,  brownish  or  reddish 

1  Ueber  Lungen-Aktinomykose,  Inaug.  Diss.,  Leipzig,  1893. 

2  Ueber  Aktinomykose,  Virchow's  Arch.,  Bd.  cxlvi.  p.  1. 

3  Virchow's  Arch.,  1906,  clxxxiv,  491.  4  Loc.  cit. 
6  Korrcspondcnzbl.  f.  schw.  Aerzte,  1889. 


380  DISEASES  OF  THE  LUNGS 

granulation  tissue.  Within  the  centre  of  the  cavity  a  communicating 
and  at  times  dilated  bronchus  may  be  found.  The  bronchial  wall  is 
usually  reddened  and  contains  pus.  More  extensive  local  or  lobar 
involvement  results  in  the  formation  of  dense  inelastic,  partially  or 

wholly  airless,  grayish  or  reddish-gray  areas  of  infiltration,  in  which 
are  found  larger  or  smaller  cavities  connecting  with  the  bronchi  and 
with  each  other  by  narrow,  complicated  fistulous  channels.  Extensive 
losses  of  substance  are  uncommon.  At  times,  however,  ulceration 
progresses  to  a  marked  degree.  An  abundant  connective-tissue 
formation  is  usually  a  striking  feature,  and  leads  to  contraction  of 
the  affected  region.  Within  the  cavities  and  also  in  the  purulent 
contents  of  the  bronchi,  actinomyces  granules  are  found. 

Microscopic  examination  of  the  contents  of  the  cavities  shows  pus 
cells,  red  blood  corpuscles,  free  fat  and  fatty  acid  crystals,  detritus 
and  isolated  or  conglomerate  masses  of  branching  Gram-staining 
filaments,  as  well  as  the  club-bearing  actinomyces  granules.  The 
primary  lesions  probably  consist  of  catarrhal  desquamation  of  the 
bronchial  mucous  membrane  through  which  the  organism  finds  its 
way  into  the  submucosa  and  peribronchial  tissues.  Here  and  in  the 
neighboring  alveoli,  there  is  round-celled  infiltration,  proliferation 
of  the  alveolar  epithelium  and  the  interstitial  connective  tissue. 
Grayish-red  nodules  are  thus  formed,  the  centre  of  which  soon  under- 
goes necrosis  and  softening,  while  at  the  periphery  an  abundant, 
vascular  connective-tissue  proliferation  more  or  less  completely  invests 
the  process.1  In  stained  sections,  multiple,  isolated  or  confluent 
abscesses  are  found,  within  few  or  many  of  which  are  radiating  club- 
bearing  actinomyces  colonies.  Between  and  within  the  pus  cells, 
few  or  many  isolated  branching  filaments  may  be  seen.  Serial  section 
may  be  necessary  to  demonstrate  the  colonies. 

There  is  no  noteworthy  difference  between  primary  pulmonary 
actinomycosis  and  that  secondary  form  of  the  disease  arising  by 
extension  from  neighboring  organs.  A  distinction  between  the  two 
forms  may  be  difficult  or  impossible.  In  general,  however,  a  more 
extensive  destructive  and  indurative  process  may  be  expected  at  the 
site  of  the  primary  focus,  although  this  is  not  invariably  true,  as  the 
earliest  lesions  may  be  partially  or  wholly  healed  by  replacement  with 
scar  tissue.  In  the  early  stages  of  metastatic  pulmonary  invasion, 
numerous  scattered  miliary  nodules  may  be  found  throughout  the 
lungs,  or  larger  wedge-shaped  subpleural  areas,  the  further  evolution 
of  which  takes  place,  as  already  described  for  the  primary  form  of  the 
disease. 

The  involvement  of  neighboring  organs  by  direct  extension  is  a 
striking  feature  of  the  disease.  Invasion  of  the  pleura  is  almost  invari- 
able, usually  leading  to  the  formation  of  adhesive  pleurisy.  Small 
and  encysted  serofibrinous,  hemorrhagic  or  purulent  pleurisy  occa- 

1  Baumgarten,  quoted  from  v.  Koranyi,  Nothnagel  Spec.  Path.  u.  Ther.,  1897,  Bel.  i, 
p.  108. 


PULMONARY  ACTINOMYCOSIS  381 

sionally  follows.  Invasion  of  the  peripleural  tissue  is  common.  Erosion 
of  the  ribs,  perforation  of  the  intercostal  spaces  in  one  or  more  places, 
and  superficial  thoracic  abscesses  are  often  found.  Invasion  of  the 
pericardium,  the  mediastinum  with  erosion  of  the  vertebrae,  extension 
downward  through  the  diaphragm  leading  to  subdiaphragmatic, 
hepatic  and  perinephritic  abscesses  are  not  infrequently  observed. 
Infection  of  the  heart  muscle  may  also  take  place.  Metastatic  dis- 
tribution may  lead  to  abscess  formation  in  any  organ  of  the  body, 
more  especially  in  the  spleen  and  kidney,  less  often  in  the  brain. 
Amyloid  may  follow  the  long-continued  suppuration. 

Symptoms  and  Physical  Signs. — The  clinical  picture  is  variable. 
The  onset  of  the  primary  pulmonary  form  is  usually  insidious.  The 
course  is  commonly  chronic,  acute  only  in  rare  instances. 

The  initial  symptoms  are  those  observed  in  other  inflammatory 
affections  of  the  bronchopulmonary  system,  and  closely  resemble 
tuberculosis.  There  is  a  history  of  cough  with  gradually  increasing 
sputum.  Dyspnea  at  first  slight,  but  of  gradually  increasing  degree, 
is  common.  Slight  elevation  of  temperature  is  almost  constantly 
observed.  Pleural  pain  is  a  feature  in  a  large  proportion  of  the  cases. 
As  the  disease  progresses,  the  cough  becomes  more  troublesome.  The 
fever  is  more  marked  and  irregular,  intermittent  or  remittent.  Loss 
of  weight  and  strength,  pallor,  night  sweats  and  emaciation  gradually 
ensue. 

The  sputum  presents  no  distinctive  features,  other  than  the  actino- 
myces  granules.  In  Riitimeyer's1  case,  the  patient  made  the  unusual 
observation  of  a  sensation  as  if  the  mouth  were  full  of  sand  and  of 
grating  between  the  teeth  from  the  presence  of  the  granules.  The 
sputum  is  at  first  scanty,  whitish  and  mucoid  or  mucopurulent.  As 
the  disease  progresses,  it  becomes  more  purulent  and  of  a  yellowish  or 
greenish  color.  It  is  commonly  odorless,  but  may  be  fetid.  In  some 
instances,  it  is  distinctly  foul.  The  amount  is  variable  and  usually 
small  throughout  the  course  of  the  illness.  The  expectoration  com- 
monly takes  place  throughout  the  day,  rather  than  in  attacks  at  long 
intervals,  as  in  ordinary  bronchiectasis  or  pulmonary  abscess.  Large 
amounts  are  occasionally  observed,  and  at  times  as  much  as  one-half 
to  one  liter  in  the  twenty-four  hours.  Blood  in  the  sputum  is  men- 
tioned in  fully  one-half  of  the  more  carefully  reported  cases  in  the 
literature.  It  may  occur  as  bloody  streaks  or  masses,  and  the  sputum 
may  in  consequence  be  bright  red,  rusty,  brownish  or  blackish  in 
color.  In  rare  instances  the  sputum  resembles  currant  jelly.  Small 
amounts  of  fresh  blood  are  occasionally  observed. 

Large  amounts  of  fresh  blood  have  been  recorded  in  rare  instances. 
In  Rieke's2  case  a  hemorrhage  amounting  to  one-third  of  a  liter,  after 
pulmonary  symptoms  had  lasted  for  about  three  months,  appeared 

1  Berl.  klin.  Woch.,  1889,  p.  68. 

2  Ein  Fall  von  primarer  Lungenaktinomykose  mit  totlicher  Blutung,  Inaug.  Diss., 
Kiel,  1903. 


382  DISEASES  OF  THE  LUNGS 

to  hasten  the  fatal  termination.  In  Bulling  and  Kulhnann's1  case 
hemoptysis  was  an  early  symptom.  A  recurrence,  amounting  to  three- 
quarters  of  a  liter,  terminated  an  illness  of  about  a  year  and  a  half. 
In  one  of  the  Massachusetts  General  Hospital  cases  (No.  109,915), 
three  hemorrhages,  each  of  a  liter  or  more,  occurred  during  the  course 
of  ;i  primary  pulmonary  actinomycosis.  The  first  bleeding  took  place 
during  the  second  month  of  pulmonary  symptoms.  Club-bearing 
actinomyces  granules  were  found  in  the  sputum,  but  no  tubercle 
bacilli.  Hemoptysis  as  an  initial  symptom  has  not  so  far  as  I  know 
been  observed. 

In  Finckh's2  case  a  primary  pulmonary  actinomycosis  with  thoracic 
perforation  was  complicated  with  fibrinous  bronchitis,  and  in  the 
fibrinous  casts  of  the  bronchi  numerous  actinomyces  granules  were 
found.  Elastic  tissue  is  occasionally  found  in  the  sputum,  but  appar- 
ently less  often  than  in  pulmonary  tuberculosis. 

Israel3  has  divided  the  clinical  course  of  the  diseases  into  three 
stages.  In  the  first  or  bronchopulmonary  stage,  the  process  does  not 
extend  beyond  the  limits  of  the  pulmonary  tissue.  Involvement 
of  the  pleura  marks  the  beginning  of  the  second  or  'pleurotlioraeic, 
while  invasion  of  the  thoracic  wall  terminates  in  the  third  or  fistulous 
stage.  The  classification  presents  a  useful  picture  of  the  usual  progress 
of  the  disease.  In  most  clinical  cases,  however,  the  exact  limits  of  the 
process  cannot  be  accurately  determined.  This  is  especially  true  of  the 
first  two  stages. 

The  disease  is  seldom  recognized  in  the  early  part  of  its  course. 
Such  pulmonary  symptoms  as  have  already  been  described  may  be 
present.  Physical  examination  may  be  negative  or  the  physical  signs 
of  bronchial  catarrh,  pulmonary  infiltration  or  cavity  formation  may 
be  established.  Canali's4  case,  often  quoted  as  an  instance  of  bronchial 
actinomycosis,  probably  belongs  in  the  pulmonary  group.  The  patient, 
a  girl  aged  fifteen  years,  gave  a  history  of  cough  and  expectoration, 
with  frequent  febrile  attacks  for  a  period  of  eight  years.  The  sputum 
was  foul  and  contained  actinomyces  granules.  Examination  failed  to 
show  signs  other  than  those  of*  a  diffuse  bronchitis.  Involvement 
of  the  pulmonary  tissue  cannot  be  excluded  and  the  further  course 
of  the  disease  is  unknown. 

At  times,  the  symptoms  of  pleural  invasion  are  the  first  indication 
of  the  disease.  This  is  more  likely  if  the  pulmonary  process  is  per- 
ipherally placed.  With  central  lesions,  months  may  elapse  before  the 
pleura  is  reached.  Pleural  involvement  may  be  latent.  There  may 
be  only  slight  and  occasional  pain,  or  the  pain  may  be  severe  and 
accompanied  by  high  fever  and  chills.  Pleural  friction  may  be  heard. 
Limitation  of  thoracic  motion,  retraction  of  the  side,  narrowing  of  the 

1  Kin  Fall  von  Lungenaktinomykose,  Berl.  klin.  Woch.,  21  Okt,,  1907. 

2  Beitriige  z.  klin.  Chir.  Tubingen,  1903-04,  vol.  xli. 

3  Klin.  Beitrage  z.  Kenntniss  der  Aktinom.  des  Menschen.,  Berlin,  1885,  Hirsehwald. 

4  La  broncho-actinomycosi  nell'  uomo.,  Rivista  clinica,  Bologna,  1882. 


PULMONARY  ACTINOMYCOSIS  383 

intercostal  spaces,  dislocation  of  the  heart  toward  the  lesion,  and 
absence  of  the  diaphragm  shadow  may  indicate  an  adhesive  pleurisy. 
Dulness,  diminished  breathing,  voice,  whisper,  and  tactile  fremitus 
may  be  present  as  a  result  of  thickened  pleura.  An  accumulation  of 
encysted  or  free  serofibrinous,  purulent  or  hemorrhagic  effusion  may 
be  found.  The  small  and  circumscribed  purulent  exudates  are  more 
common.  Retraction  of  the  affected  side  is  an  important  sign  and  may 
be  observed  with  or  without  an  effusion. 

It  is  uncommon  for  the  disease  not  to  exceed  the  limits  of  the  pleura 
and  perforate  the  chest  wall.  Cases  without  perforation  of  the  thoracic 
wall,  have,  however,  been  reported,  among  others  by  Ponfick,1  Ilebb,2 
Hanau,3  Heusser,4  Butler,5  Kashiwamura,6  von  Graff,7  Schlagenhaufer,8 
and  Bulling  and  Rullmann.9  An  unusually  early  stage  of  the  disease 
was  observed  at  the  Massachusetts  General  Hospital.  The  patient 
(Autopsy  1488),  a  man  aged  forty-six  years,  with  a  family  history  of 
tuberculosis  and  of  cough  and  blood-tinged  sputum  for  only  twenty-two 
days,  was  found  at  autopsy  to  have  an  organizing  pneumonia  with 
abscess  and  cavity  formation  in  the  right  upper  and  lower  and  left 
lower  lobes.  The  pleural  cavities  were  free  from  fluid.  The  lungs  were 
bound  to  the  parietal  pleura  by  a  few  adhesions.  In  three  of  the  pul- 
monary cavities,  typical  club-bearing  actinomyces  colonies  wTere  found 
in  stained  sections  of  the  tissue.  The  right  lung  also  showed 
tuberculosis. 

Perforation  of  the  chest  wall  is  observed  more  commonly  in  this 
than  in  any  other  form  of  pulmonary  disease.  It  was  recorded  in  82 
of  100  cases  collected  from  the  literature.  Its  occurrence  should  never 
fail  to  suggest  the  diagnosis  of  actinomycosis.  Rupture  may  occur 
at  any  part  of  the  chest.  The  abscess  may  point  in  the  neck  as  in 
Lindt's10  case  or  it  may  first  reach  the  surface  in  the  abdominal  wall. 
The  abscess  slowly  makes  its  way  from  the  peripleural  space,  between 
or  through  the  thoracic  muscles  to  the  subcutaneous  tissue.  A  flat, 
hard,  elastic,  circumscribed  or  diffuse  tumor-like  swelling  appears. 
The  overlying  skin  may  be  normal  or  dusky  red.  The  superficial 
veins  may  be  dilated.  Owing  to  the  abundance  of  the  connective- 
tissue  formation  and  the  usual  absence  of  large  accumulations  of  pus, 
the  mass  is  brawny  and  true  fluctuation  is  seldom  observed.  Small 
areas  of  softening  in  the  midst  of  indurated  tissue  may  give  rise  to 
softer,  fluctuating  and  harder,  resistant  areas  side  by  side  which  on 
palpation  make  the  surface  appear  uneven.  The  swelling  may  be 
tender.     The  inflammatory  process  is  indolent,  and  a  long  interval 

i  Breslauer  aerztl.  Zeit.,  1885,  No.  3.  2  Lancet,  1887,  i,  313. 

3  Correspondenzbl.  f.  schw.  Aerzte.,  1889,  No.  6,  p.  165. 

4  Berl.  klin.  Woch.,  25  Nov.,  1895.  5  Med.  News,  1898,  No.  17. 

6  Virchow's  Arch.,  1903,  vol.  clxxi. 

7  Zeit.  f.  Heilkunde,  1904,  25,  Abt.  path.  Anat. 

*  Virchow's  Arch.,  1906,  clxxxiv,  491.  9  Berl.  klin.  Woch.,  21  Okt.,  1907. 

10  Ein  Fall  von  primarer  Lungenspitzenactinomykose,  Korrespondenzbl.  f.  schw. 
Aerzte,  1889. 


384  DISEASES  OF  THE  LUNGS 

may  elapse  before  rupture  of  the  skin  takes  plaee.  Perforation  is 
likely  to  occur  in  several  plaees.  In  the  absence  of  extension  from  the 
neck,  actinomycosis  of  the  chest  wall  should  always  be  regarded  as 
proceeding  from  a  primary  pulmonary  focus.  Israel1  reports  an  instance 
of  subcutaneous  emphysema  in  the  course  of  pulmonary  actinomycosis. 

Extension  may  also  take  place  into  the  prevertebral  space,  the  peri- 
cardium or  the  abdomen.  The  patient's  general  condition  gradually 
fails.  Increasing  pallor,  fever  of  an  irregular  type  and  night  sweats 
are  commonly  present.  Chills  may  also  occur.  Metastases  in  the 
liver,  spleen,  heart  and  brain  may  be  latent  or  take  place  with  the 
clinical  features  of  pyemia.  Metastatic  abscesses  in  the  skin  are  occa- 
sionally observed  and  present  the  appearances  already  described  for 
the  thoracic  phlegmon.  Amyloid  of  the  liver  and  spleen  may  cause 
palpable  enlargement  of  these  organs  in  the  course  of  long-continued 
suppuration.  Death  may  be  due  to  progressive  marasmus  or  to 
metastatic  involvement  of  a  vital  organ. 

Diagnosis. — Primary  pulmonary  actinomycosis  is  often  unrecog- 
nized. During  the  period  before  perforation  of  the  chest  wall  takes 
place,  the  disease  closely  simulates  other  more  common  pulmonary 
affections,  and  the  diagnosis  cannot  be  made  without  the  demonstra- 
tion of  actinomyces  in  the  sputum.  It  should  therefore  be  an  invariable 
rule  to  search  for  actinomyces  granules  in  the  sputum  from  all  cases 
with  pulmonary  suppuration. 

In  the  early  stages  of  the  development  of  the  primary  pulmonary 
form  there  are  no  distinctive  clinical  features.  The  gradually  increasing 
cough,  mucopurulent  or  purulent  and  at  times  bloody  sputum,  dyspnea, 
pleural  pains,  occasional  fever,  night  sweats,  failing  health  and  strength, 
physical  signs  of  local  bronchitis,  pulmonary  infiltration,  or  cavity 
formation,  with  or  without  involvement  of  the  pleura,  naturally 
suggest  pulmonary  tuberculosis.  Actinomycosis  is  usually  basal, 
but  attacks  one  and  even  both  apices  in  rare  instances.  The  absence 
of  a  family  history  of  tuberculosis  or  known  opportunity  for  contagion, 
the  failure  to  find  tubercle  bacilli  in  the  sputum  after  careful  and 
repeated  search  and  negative  tests  with  tuberculin,  make  actinomy- 
cosis more  probable,  but  actinomycosis  and  tuberculosis  may  coexist. 
The  demonstration  of  the  one,  therefore,  does  not  serve  to  exclude 
the  other.  Non-tuberculous  lesions  such  as  abscess,  gangrene,  bron- 
chiectasis and  interstitial  pneumonia  must  also  be  considered,  but 
whether  they  are  due  to  actinomyces  or  to  simpler  infection  cannot 
be  determined  without  the  sputum  examination.  A  shorter  and  more 
stormy  course,  relatively  less  abundant  sputum  and  more  marked 
thoracic  retraction  is  perhaps  more  common  with  actinomycosis,  but 
such  features  cannot  be  relied  upon  in  the  differentiation. 

The  presence  of  a  circumscribed  thoracic  swelling,  of  the  character 
already  described,  is  one  of  the  most  important  physical  signs  of  the 

1  Deut.  Med.  Woch.,  1906,  xxxii,  166. 


PULMONARY  ACTINOMYCOSIS  385 

disease,  and  with  its  appearance  a  probable  diagnosis  of  actinomycosis 
can  be  made  before  the  actinomyces  granules  are  demonstrated. 
Abscesses  due  to  a  perforating  empyema  or  tuberculosis  of  the  ribs 
are  more  fluctuant  and  less  brawny  and  uneven.  Malignant  disease, 
especially  sarcoma  primary  in  the  chest  wall,  lung  or  pleura  with 
extension  or  metastasis  outward,  is  less  likely  to  be  accompanied  by 
suppurative  pulmonary  lesions.  The  growth  itself  is  more  often 
rounded,  harder  and  less  fluctuant.  Other  metastases  may  be  found. 
Tuberculous  or  syphilitic  periostitis  may  be  a  possible  cause  of  con- 
fusion. Local  prominence  of  the  chest  wall  may  be  noted  with  pul- 
monary or  pleural  echinococcus.  The  actinomycotic  nature  of  the 
swelling  in  question  may  be  established  by  the  demonstration  of 
the  characteristic  granules  obtained  by  puncture  or  expressed  from 
discharging  sinuses.  Aneurysm  of  the  thoracic  aorta  should  be 
considered  in  the  presence  of  tumors  which  appear  in  the  supracardiac 
or  lower  left  paravertebral  regions. 

Actinomyces  granules  are  readily  recognized.  Their  identification 
has  already  been  considered.  Only  typical  club-bearing  colonies 
should  be  regarded  as  actinomyces  when  making  a  diagnosis  from  fresh 
specimens.  Colonies  without  clubs  can  be  so  regarded  only  after  their 
full  biologic  identity  has  been  established.  This  involves  isolation 
in  pure  culture.  Unless  care  is  taken,  grayish  or  yellowish  granules, 
frequently  found  in  the  sputum  and  composed  of  leptothrix  or 
streptothrix  filaments  with  entangled  cells  may  be  mistaken  for 
actinomyces.  Leptothrix  filaments  are  unbranched  rods,  thicker 
than  actinomyces  and  stain  after  Gram.  The  streptothrix  filaments 
appear  as  slender,  branching,  Gram-staining  threads,  which  resist 
decolorization  by  weak  acids.  The  absence  of  the  characteristic 
"clubs"  from  such  granules  is  the  most  trustworthy  means  of  differ- 
entiation. 

Prognosis. — This  is  unfavorable.  The  prospect  for  recovery  is  only 
little  better  with  pulmonary  actinomycosis  than  with  a  malignant 
tumor  of  the  lung.  Pulmonary  tuberculosis  is,  by  comparison,  a  mild 
disease.  The  cases  usually  prove  fatal  in  the  course  of  six  months  to 
a  year.  A  duration  of  from  two  to  three  years  is  at  times  observed. 
One  instance  of  apparent  spontaneous  recovery  has  been  reported 
by  Butler.1  There  was  cough  and  offensive  expectoration  in  which 
Hodenpyl  found  actinomyces  granules.  Recovery  took  place  in  the 
course  of  two  to  three  months.  The  case  deviates  from  the  ordinary 
type  of  the  disease  in  the  absence  of  thoracic  perforation,  and  it  is 
unfortunate  that  the  granules  were  not  described.  Surgical  treatment 
makes  the  prognosis  less  hopeless,  but  thus  far  only  six  other  cases- 
are  known  to  have  recovered. 

Prophylaxis. — Our  present  knowledge  does  not  permit  the  formula- 
tion of  adequate  preventive  measures.    The  supposition  that  actino- 

1  Med.  News,  1898,  No.  17. 

2  See  page  386.     Hamm's  case  is  excluded. 
25 


386  DISEASES  OF  THE  LUNGS 

myces  normally  exists  in  the  buccal  cavity,  the  occasional  association 
of  the  disease  about  the  jaw  with  carious  teeth,  and  the  association 
of  the  pulmonary  form  with  the  inhalation  of  foreign  bodies,  makes 
reasonable  the  suggestion  that  the  mouth,  and  especially  the  teeth, 
should  be  kept  clean,  and  that  when  possible  foreign  bodies  should 
be  early  removed  from  the  bronchi.  It  is  not  improbable  that  the 
establishment  of  anaerobic  conditions,  as  in  a  tooth  cavity  filled  with 
accumulated  food,  or  the  aspiration  of  infected  material  into  the  deeper 
parts  of  the  lungs,  favors  the  development  of  the  organisms.  It  is 
possible  from  this  point  of  view  that  careless  dentistry  may  convert 
a  carious  tooth  into  an  anaerobic  culture.  Punctured  wounds  about 
the  buccal  cavity  may  likewise  favor  the  development  of  the 
organism. 

Treatment. — This  is  unsatisfactory.  Iodid  of  potash  is  said  to 
cure  53  per  cent,  of  the  cases  in  cattle.  Favorable  results  have  been 
reported  in  man  from  its  use  in  actinomycosis  of  the  jaw  and  abdomen. 
Iodid  of  potash  is  not  known  to  have  cured  an  undoubted  case  of  the 
pulmonary  form  of  the  disease  in  man. 

In  Netter's1  case,  with  a  left  serofibrinous  pleurisy  and  actinomy- 
cosis of  the  chest  wall,  apparently  secondary  to  infection  of  the  medias- 
tinum, recovery  followed  the  administration  of  iodid  of  potash  in 
doses  up  to  6  grams  a  day — 61  grams  in  all — during  a  period  of  twenty- 
seven  days.  Pulmonary  infection  was  not  established.  In  one  of  the 
cases  reported  by  Prutz2  with  pulmonary  actinomycosis,  disappearance 
of  the  granules  from  the  sputum  and  improvement  of  the  general 
condition  followed  numerous  operations  on  an  abscess  of  the  thoracic 
wall  and  the  administration  of  not  less  than  4000  grams  of  iodide  of 
potash  in  the  course  of  two  years.  The  patient  was  discharged  with 
sinuses. 

Wynn3  treated  with  vaccines  a  case  of  empyema,  in  the  pus  of  which 
granules  were  found.  It  is  improbable  that  he  could  have  isolated  true 
actinomyces  by  the  cultural  methods  employed.  The  use  of  vaccines 
deserves  a  trial,  however,  in  so  hopeless  a  disease. 

The  results  of  operative  procedures  are  more  promising.  The 
instances  of  reported  recovery  following  operation  are  as  follows: 

Schlange4  has  reported  two  favorable  cases.  Actinomyces  granules 
were  found  in  the  sputum  from  both.  In  the  first,  a  thoracic  abscess 
containing  the  granules  was  incised  and  two  ribs  were  resected  without 
opening  the  pleura.  There  was  no  evidence  of  actinomycosis  six 
years  after  the  operation.  In  the  second  case,  actinomyces  granules 
were  found  in  a  large  pleural  exudate.  Apparent  recovery  followed 
thoracentesis,  although  the  patient  still  presented  a  fistula  in  the  lower 
abdominal    region  five  years    afterward   and    suffered   from   severe 

1  Bull,  et  mem.  de  la  Soc.  Med.  des  Hop.  de  Paris,  Seance  du  3  nov.,  1893. 

2  Mitt.  a.  d.  Grenzg.  d.  Med.  u.  Chir.,  1899,  Bd.  iv,  p.  63. 

3  British  Med.  Jour.,  May  11,  1907. 

4  Langenbeck's  Arch.  f.  klin.  Chir.,  1892,  vol.  xliv. 


PULMONARY  ACTINOMYCOSIS  :J>S7 

attacks  of  cough  every  few  weeks.     No  actinomyces  could  then  be 
found  in  the  sputum. 

Jakowski1  reports  a  case  in  which  the  presence  of  actinomyces  was 
determined  by  puncture  of  a  thoracic  phlegmon.  The  abscess  was 
incised  by  Jawdynski,  the  sixth  to  the  ninth  ribs  were  resected  and  an 
actinomycotic  pulmonary  cavity  between  the  anterior  and  midaxillary 
line  was  thus  opened.  The  walls  of  the  cavity  were  extirpated  by 
means  of  the  cautery  and  recovery  followed. 

Karewski2  has  reported  a  fourth  instance.  Pulmonary  symptoms 
had  persisted  for  four  months,  and  the  thoracic  wall  was  invaded.  A 
cavity  with  actinomycotic  granulations,  pus  and  granules  was  opened 
by  resection  of  the  sixth  rib  from  the  axilla  to  the  sternum.  All  infil- 
trated regions  were  destroyed  by  means  of  the  cautery,  leaving  a  pul- 
monary cavity  the  size  of  the  fist,  partial  closure  of  which  was  effected 
by  Thiersch's  method  of  skin-grafting.  This  patient  was  well  more 
than  ten  years  after  the  operation. 

Brentano's3  case  was  operated  for  a  tumor  containing  actinomyces 
granules  in  the  left  chest  wall.  The  eighth,  ninth,  and  tenth  ribs  were 
resected  from  the  mammillary  to  the  midaxillary  line.  A  pulmonary 
lesion  was  not  demonstrated.  The  tumor  was  incised,  curetted  and 
cauterized.  The  patient  was  still  well  one  and  one-half  years  later, 
according  to  Karewski4  report. 

Hamm5  reports  a  case  of  pulmonary  actinomycosis  with  an  encap- 
sulated empyema,  as  fully  recovered,  and  Karewski6  states  that  the 
case  was  still  well  one  year  and  three  months  after  the  operation. 
The  case  can  be  accepted  only  with  reserve,  since  details  concerning 
the  diagnosis  and  the  operative  procedures  are  lacking. 

Opotkin7  reports  a  case  of  Rasumowsky's  with  pulmonary  abscess 
due  to  actinomycosis.  The  thoracic  wall  was  perforated  between  the 
fifth  and  sixth  ribs  on  the  right  side.  Six  centimeters  of  the  sixth  rib 
were  resected  and  a  cavity  the  size  of  an  orange  was  found  behind  the 
thoracic  wall,  extruding  into  the  lung.  Actinomyces  were  not  found 
in  the  sputum.  The  cavity  was  scraped  out  and  cleaned.  Iodid  of 
potash  was  also  given.  After  several  operations,  during  the  course  of 
five  years  of  observation,  the  process  had  very  largely  healed,  only 
a  fistulous  passage  remaining. 

Cases  in  which  metastases  have  already  occurred  are  not  amenable 
to  surgery,  and  it  is  therefore  important  that  the  diagnosis  should  be 
made  while  the  disease  is  still  local  and  circumscribed.  In  the  esti- 
mation of  the  amount  of  pulmonary  involvement  and  the  detection 
of  lesions  not  otherwise  to  be  found,  examination  by  means  of  the 

1  Gazeta  Lekarska,  1897,  No.  1,  Ref.  Centr.  f.  Chir.,  1897,  No.  28. 

2  Berl.  klin.  Woch.,  1898,  and  Langenbeck's  Arch.  f.  klin.  Chir.,  1907,  vol.  Ixxxiv. 

3  Deut.  med.  Woch.,  1906,  xxxii,  165. 

4  Langenbeck's  Arch.  f.  klin.  Chir.,  1907,  vol.  Ixxxiv. 
6  Deut.  med.  Woch.,  1906,  p.  941. 

6  Langenbeck's  Arch.  f.  klin.  Chir.  1907,  vol.  Ixxxiv 

7  Arch.  f.  klin.  Chir.,  1908-09,  lxxxviii,  469. 


388  DISEASES  OF  THE  LUNGS 

x-rays  may  be  of  great  service.  Latent  metastatic  distribution  may 
take  place  and  operation  in  an  apparently  hopeful  condition  prove 
unsuccessful. 

The  chances  of  metastasis  increase  with  the  duration  of  the  disease, 
and  the  earlier  the  operation  is  undertaken  the  more  likely  is  it  to  be 
successful.  It  is  much  to  be  hoped  that  pulmonary  actinomycosis  may 
be  surgically  treated  before  thoracic  perforation  takes  place,  but  even 
after  this  has  occurred  the  conditions  may  still  be  amenable  to  opera- 
tion. In  Jakowski's,  Karewski's,  and  Brentano's  cases,  an  interval 
of  several  months,  of  four  months  and  of  three  months,  respectively, 
had  already  elapsed  between  the  beginning  of  pulmonary  symptoms 
and  the  appearance  of  a  thoracic  tumor,  and  yet  recovery  followed  radi- 
cal operation.  Even  a  long  previous  duration  is  compatible  with 
local  and  circumscribed  lesions,  and  unless  metastases  can  be  demon- 
strated, the  case  should  not  be  regarded  as  hopeless.  In  Moosbrugger's1 
case,  with  pulmonary  symptoms  for  two  years  and  a  thoracic  tumor 
for  nine  months,  the  disease  was  found  at  autopsy  to  be  limited  to  the 
lung,  the  mediastinum  and  pericardium.  In  Heinzelmann's2  patient, 
likewise,  the  pulmonary  symptoms  had  lasted  for  two  and  one-quarter 
years,  and  a  thoracic  swelling  for  about  seven  months,  while  at  autopsy 
other  organs  than  the  lung,  the  epicardium  and  myocardium  were 
unaffected. 

The  possibility  of  surgical  relief  is  also  illustrated  by  Karewski's 
success  in  completely  curing  the  local  disease  by  operation  in  three  of 
his  series,  although  the  patients  finally  died — one  from  amyloid  and 
extension  into  inaccessible  regions,  the  other  two  from  metastases. 

Such  conservative  methods  as  simple  incision  and  drainage  of  the 
superficial  thoracic  plegmon  have  usually  served  only  temporarily, 
if  at  all,  to  delay  the  progress  of  the  disease.  Karewski  believes  that 
pulmonary  actinomycosis  should  be  treated  rather  as  a  malignant 
growth  by  extirpation  than  as  an  abscess  by  drainage.  He  recommends 
the  free  opening  and  destruction  of  all  fistulous  passages,  the  resection, 
if  necessary,  of  several  or  many  ribs  to  find  the  channels  of  communi- 
cation with  the  lung  and  the  discovery  and  extirpation  of  the  primary 
pulmonary  infection.  Firm  indurated  tissue  should  be  extirpated  or 
removed,  regardless  of  functionally  important  muscles.  Only  that 
which  is  macroscopically  sound  or  a  delimiting  wall  without  granules 
should  be  spared.  Further  operations  will  be  necessary  if  granules 
are  later  found  in  the  discharge  from  the  wounds  of  operation.  Firm 
pleural  adhesions  usually  lessen  the  danger  of  artificial  pneumothorax. 
The  danger  of  hemorrhage  is  commonly  slight,  and  bleeding,  when  it 
occurs,  can  be  controlled  with  the  cautery. 

1  Beitr.  z.  klin.  Chir.,  Bd.  ii.  2  Ibid.,  Bd.  xxxix. 


CHAPTER  XXII. 
PULMONARY  STREPTOTHRICOSLS. 

Under  this  term  may  be  included  pulmonary  infection  with  branch- 
ing filamentous  organisms,  the  more  important  characters  of  which 
are  described  below.  Much  difference  of  opinion  prevails  regarding 
the  members  of  this  group.  Most  writers  place  actinomyces  as  a 
species,  but  it  appears  to  have  sufficiently  distinctive  characters  to 
justify  generic  rank.  The  term  streptothrix,  in  spite  of  technical 
objections,  is  justified  by  common  usage,  and  is  to  be  preferred  to 
atypical  actinomyces,  oospora,  pseudotubercle  bacillus,  cladothrix, 
or  nocardia.  A  considerable  number  of  distinct  species  are  probably 
responsible  for  infection  in  this  group.  The  article  by  Musgrave, 
Clegg  and  Polk1  contains  an  extensive  bibliography. 

Etiology. — The  predisposing  factors  influencing  infection  are  little 
known.  Contagion  has  not  been  established.  Certain  species  have 
been  found  widely  distributed  in  nature,  i.  e.  in  the  air,  water,  soil  and 
on  foodstuffs,  and  the  biologic  characters  of  the  pathogenic  forms 
suggest  a  habitat  outside  the  body,  so  that  it  may  be  regarded  as 
likely  that  pulmonary  infection  takes  place  by  inhalation. 

The  Microorganisms. — In  fresh  material  obtained  from  the  lesions, 
the  organisms  are  found  as  isolated  slender  filaments  or  a  loose  net- 
work of  filaments  which  stain  with  the  ordinary  analine  dyes  homo- 
geneously, or  present  a  granular  or  beaded  appearance.  Aggregation 
into  clusters  or  colonies  of  interlacing  filaments  is  often  observed. 
True  branching  may  be  seen  in  few  or  many  of  the  filaments.  They 
are  Gram  positive  and  show  a  varying  degree  of  resistance  to  decolori- 
zation  by  acids  after  being  stained  with  carbol-fuchsin.  The  acid- 
fastness  is  usually  less  than  that  of  the  tubercle  bacillus,  but  in  some 
instances  the  organisms  have  been  as  acid-fast  as  the  tubercle  bacillus. 
Some  resistance  to  decolorization  by  alcohol  has  also  been  noted. 
Growth  usually  takes  place  readily  but  slowly  on  all  culture  media 
under  aerobic  conditions  and  at  room  as  well  as  body  temperature. 
Cultural  peculiarities  are  variable.  Under  the  microscope  young 
colonies  usually  show  the  presence  at  the  periphery  of  radially  arranged 
and  branching  filaments.  In  smears  from  cultures,  rods  with  conical 
extremities  may  be  observed  as  well  as  the  slender  branching  filaments. 
Bacillary  and  coccus-like  forms  may  arise  by  the  breaking  up  of  the 
filaments  in  fresh  material  and  in  older  cultures.  Surface  growth  may 
be  seen  on  bouillon  or  the  formation  of  ball-like  masses  at  the  bottom 
of  the  tube  without  clouding  of  the  medium.    The  results  of  animal 

1  Philippine  Jour.  Sci.,  1908,  iii,  447. 


390  DISEASES  OF  THE  LUNGS 

experiments  are  inconstant.  In  some  instances,  local  abscesses  are 
formed  after  subcutaneous  or  intraperitoneal  injection  or  widely 
disseminated,  yellowish,  miliary  tubercle-like  nodules  after  intravenous 
inoculation.  The  nodules  show  on  histologic  examination  infiltration 
with  leukocytes  and  more  or  less  extensive  central  necrosis.  Spore 
formation  (chain  sporulation)  is  thought  to  occur. 

Pathology. —The  pulmonary  lesions  ascribed  to  these  organisms 
include  bronchopneumonia,  abscess,  gangrene,  bronchiectasis  and 
indurative  processes.  Fibrinous  pleurisy  and  empyema  are  also 
observed.  Perforation  of  the  chest  wall  may  occur.  In  the  cases 
described  by  Flexner1  and  Lohlein2  tubercle-like  nodules  were  found 
in  the  lung.  Changes  in  the  bronchial  wall  leading  to  bronchiectasis 
were  a  feature  of  the  cases  described  by  Norris  and  Larkin3  and  Horst4. 
In  the  involved  tissue,  the  organisms  are  found  scattered  diffusely 
or  form  loosely  aggregated  masses.  Granules  or  masses  of  closely 
packed  interlacing  filaments  with  radially  disposed  club-shaped,  eosin 
staining,  peripheral  bodies,  such  as  are  seen  in  actinomycosis,  have  not 
been  observed  in  streptothricosis. 

Metastatic  lesions  may  arise  in  various  organs  of  the  body  in  con- 
sequence of  perforation  of  the  pulmonary  veins.  Invasion  of  the  cen- 
tral nervous  system  with  the  formation  of  cerebral  abscesses  is  not 
infrequent.  Multiple  subcutaneous  abscesses  are  also  observed. 
Invasion  of  the  pericardium,  myocardium,  kidney,  liver,  spleen, 
muscles,  peritoneum  and  lymph  glands  has  been  noted,  in  connection 
with  pulmonary  involvement.  Streptothrix  has  been  cultivated  from 
the  heart's  blood  after  death  by  Lohlein.5  Blood  cultures  were  positive 
in  eight  successive  trials  in  a  case  reported  by  Schottmuller  and  Frankel6 
Infection  in  this  instance  followed  the  bite  of  a  rat,  and  the  only  evi- 
dence of  pulmonary  involvement  was  transient  bronchitis.  The 
patient  recovered. 

Symptoms. — These  are  varied,  and  may  be  either  acute  or  chronic. 
The  clinical  picture  may  resemble  pulmonary  tuberculosis,  broncho- 
pulmonary suppuration,  abscess  or  gangrene  and  interstitial  pneu- 
monia. Cough,  more  or  less  abundant  purulent  sputum,  at  times 
streaked  with  blood,  dyspnea  and  pain,  with  fever,  night  sweats, 
loss  of  weight  and  strength  and  emaciation  may  be  observed.  Hemop- 
tysis occurred  in  Jamieson's7  case.  In  some  instances  the  clinical 
features  are  those  of  empyema,  and  if  the  chest  wall  is  perforated, 
actinomycosis  may  be  suggested.  In  Lohlein's  case  the  course  was 
that  of  pyemia  following  primary  bronchopneumonia. 

Diagnosis. — This  may  be  made  by  the  demonstration  in  the  sputum 
of  thread-like,  branching  organisms  which  usually  resist  decolorization 

1  Trans.  Assoc.  Amer.  Phys.,  1898,  xiii,  31.  2  Zeit.  f.  Hyg.,  1909,  Ixiii,  1. 

s  Jour.  Exp.  Med.,  1900-01,  v,  155.  4  Zeit.  f.  Heilk.,  1903,  xxiv,  157. 

6  Loc.  cit. 

6  Munch,  med.  Woch.,  1912,  No.  xxv,  1405. 

7  Australas.  Med.  Gaz.,  1907,  xxvi,  16. 


PULMONARY  STREPTOTHRICOSIS  391 

by  weak  acids  and  at  times  also  by  alcohol,  but  are  less  resistant 
against  both  acids  and  alcohol  than  the  tubercle  bacillus.  Gabbett's 
methylene-blue  solution  used  as  a  contrast  stain  after  staining  with 
carbol-fuchsin  is  useful  for  the  demonstration  of  these  organisms,  as  it 
contains  no  alcohol  and  is  an  ineffective  decolorizer.  Care  must  be 
observed  not  to  mistake  streptothrices  for  branching  tubercle  bacilli 
from  which  they  may  be  distinguished  by  their  longer,  thread-like 
form,  tendency  to  appear  in  loose  clusters  of  numerous  interlacing 
filaments,  less  resistance  to  acids,  the  greater  readiness  with  which 
they  may  be  cultivated,  cultural  peculiarities  and  the  results  of  animal 
inoculation.  From  actinomycetes  the  streptothrices  may  be  differen- 
tiated by  their  loose  rather  than  compact  colony  formation  and  the 
absence  of  radially  disposed,  club-shaped,  eosin-staining,  peripheral 
bodies.  Actinomycetes  do  not  resist  decolorization  with  acids  and 
alcohol  and  are  cultivated  with  difficulty  and  only  under  special  con- 
ditions. The  cultural  and  pathogenic  peculiarities  of  the  actino- 
mycetes and  streptothrices  are  quite  dissimilar. 

Prognosis. — This  appears  to  be  very  unfavorable,  as  all  the  cases 
of  pulmonary  infection  in  which  the  presence  of  the  streptothrix  was 
satisfactorily  established  have  died.  But  as  a  considerable  proportion 
of  the  more  authentic  instances  of  infection  have  been  the  result  of 
careful  postmortem  examinations,  it  is  possible  that  the  outlook  is 
more  favorable  than  the  previously  reported  cases  seem  to  indicate. 
In  Steele  and  Lee's1  case,  organisms  resembling  streptothrices  in 
morphology  and  staining  reaction  were  found  in  the  sputum  and  the 
patient  recovered.  Schottmuller  and  Frankel's2  report  of  recovery 
after  a  general  infection  with  these  organisms  has  already  been 
mentioned. 

Treatment. — There  is  no  specific  treatment.  Improvement  of  the 
general  health  and  nutrition,  as  in  pulmonary  tuberculosis,  is  at 
present  most  likely  to  accomplish  the  best  results.  Pulmonary 
abscesses  and  empyema  should  be  treated  on  the  same  principles 
as  apply  to  these  conditions  when  due  to  other  causes. 

1  Boston  Med.  and  Surg.  Jour.,  October  2,  1913. 

2  Loc.  cit. 


CHAPTER   XXIII. 
PULMONARY  BLASTOMYCOSIS. 

Blastomycosis  is  a  granulomatous  and  suppurative  process  involv- 
ing the  skin  and  not  infrequently  the  internal  organs  also  as  part  of  a 
systemic  infection.  The  infecting  organism  is  a  mold-fungus,  classed 
by  Ricketts1  as  belonging  to  the  species  oidium.  The  organism  is  also 
termed  monilia,  enddmyces  or  saccharomyces.  In  a  certain  number 
of  cases  the  disease  appears  to  have  originated  in  the  lungs.  The  first 
cases  were  described  by  Wernicke2  in  Buenos  Ayres,  Busse3  in  Germany 
and  by  Gilchrist  and  Stokes4  in  America.  A  survey  and  summary  of 
22  cases  of  systemic  blastomycosis  was  reported  by  Montgomery  and 
Ormsby.5    Many  of  the  following  details  are  taken  from  their  account. 

Etiology. — The  predisposing  causes  of  infection  are  unknown. 
Males  are  more  frequently  affected.  Inheritance  appears  not  to  be 
a  factor.  Contagion  has  not  been  established.  Age,  occupation,  and 
habits  seem  to  have  no  bearing  on  the  occurrence  of  the  disease. 
Unfavorable  hygienic  surroundings  have  obtained  in  many  of  the 
reported  cases.  Infection  may  take  place  by  inhalation  of  spores  from 
decaying  boards  and  walls  in  dwellings.6  In  this  country  most  of  the 
reported  cases  have  been  observed  in  Chicago  and  its  vicinity. 

Microorganism  of  the  Disease. — The  microorganism  appears  in  the 
lesions  as  an  oval  or  spherical  body  with  a  diameter  usually  of  seven 
to  twenty  microns  and  consisting  of  a  finely  granular  protoplasm, 
at  times  sporulating  and  often  vacuolated  and  inclosed  in  a  double 
contoured,,  hyaline  capsule.  Multiplication  in  the  lesions  takes  place 
either  by  budding  or,  as  is  less  often  the  case,  by  sporulation.  Prickles 
or  spines  projecting  from  the  capsule  may  be  observed  in  some 
instances.  The  organism  is  Gram-positive.  It  grows  well  on  ordinary 
culture  media  both  at  room  temperature  and  in  the  incubator  (Fig  56). 
Growth  takes  place  slowly  and  is  macroscopically  visible  in  from  two  to 
fourteen  days.  According  to  Hamburger,7  a  slightly  more  abundant 
growth  may  perhaps  take  place  on  faintly  acid  glucose-agar.  The 
growth  is  elevated,  white,  pasty,  and  yeast-like  or  waxy  on  slanted, 
solid  media.  Mycelia  and  aerial  hyphse  are  formed  under  certain 
conditions  of  cultivation.  On  examination  of  cultures,  spherical  or 
oval  budding  cells,  the  formation  of  mycelia  and  fruit-bearing  aerial 
hyphse  may  be  observed.     The  biologic  character  of  the  organism 

1  Jour.  Med.  Research,  1901,  vi,  377,  and  Trans.  Chicago  Path.  Soc,  1903-04,  vi,  113. 

2  Centralb.  f.  Bakt.,  1892,  xii,  859.  3  Ibid.,  1894,  xv,  175. 

4  Bull.  Johns  Hopkins  Hosp.,  1896,  vii,  129. 

5  Arch.  Int.  Med.,  1908,  ii,  1.     For  subsequent  cases  sec  ibid.,  1914,  xiii,  509. 

6  Arch.  Int.  Med.,  1914,  xiii,  509.  7  Jour.  Inf.  Dis.,  1907,  iv,  201. 


PULMONARY  BLASTOMYCOSIS 


393 


varies  widely  under  different  conditions.  The  organism  is  pathogenic 
for  ordinary  laboratory  animals,  but  the  results  of  inoculation  arc 
inconstant.     Lesions  when  produced  are  similar  to  those  in  man. 


Fig.  50 


Culture  four  weeks  old:  a,  on  glucose  agar;  b,  on  glycerin  agar  grown  at  room  tempera- 
ture; c,  on  glucose  agar  grown  in  incubator.    (Montgomery  and  Ormsby.) 

Fig.  57 


Sediment  from  blastomycotic  tissue  disintegrated  in  50  per  cent,  alcohol,  showing 
organisms  in  various  stages  of  budding.     (Montgomery  and  Ormsby.) 


394 


DISEASES  OF  THE  LUNGS 


The  mode  of  infection  is  uncertain,  but  so  far  as  the  pulmonary 
form  of  the  disease  is  concerned,  an  origin  by  inhalation  is  suggested 
by  the  bronchopneumonia  character  of  the  lesions.  Of  11  cases  with 
systemic  blastomycosis,  collected  by  Montgomery  and  Ormsby  the 
lungs  were  more  or  less  extensively  involved  in  all.  In  a  number  of 
cases  the  earliest  symptoms  were  pulmonary  and  blastomycetes  were 
demonstrated  in  the  sputum,  suggesting  the  respiratory  tract  as  the 
possible  portafof  entry.  Extension  probably  takes  place  by  way  of  the 
blood-stream. 

Fig.  58 


Blastomycosis  of  lung.    Gross  pathology.     (Le  Count  and  Myers.) 


Immunity- — Davis1  finds  that  male  guinea-pigs  are  more  susceptible 
to  infection  than  females.     Recovery  after  artificial  inoculation  is 

1  Jour.  Inf.  Dis.,  1911,  viii,  190. 


PULMONARY  BLASTOMYCOSIS 


395 


accompanied  by  a  low  grade  of  immunity  which  manifests  itself  by 
a  somewhat  more  speedy  recovery  from  subsequent  infections  and  by 
the  development  of  a  slight  fever  for  a  few  days  immediately  after 
reinoculations.  Repeated  injections  of  an  "extract"  of  oidiomycetes 
lead  to  the  development  of  an  immunity  in  guinea-pigs.  This  is  char- 
acterized by  the  more  rapid  walling  off  of  organisms  injected  into  the 
peritoneal  cavity  and  a  more  rapid  disappearance  of  lesions  which 
appear  in  the  testicles.  The  mode  of  defense  of  guinea-pigs  against 
oidiomycetes  injected  into  the  peritoneal  cavity  appears  to  consist  of 
phagocytosis  and  intracellular  digestion,  walling  off  and  encapsulation 
by  connective  tissue  and  a  somewhat  ill-defined  and  possibly  question- 
able unfavorable  influence  of  the  serum  upon  the  vitality  of  the 
organisms.    Specific  antibodies  appear  to  be  but  poorly  developed. 

Fig.  59 


Section  of  lung.     Large  masses  of  blastomycetes.      (Fontaine,  Haase,  and  Mitchell.) 


Pathology. — The  pathologic  features  closely  resemble  tuberculosis, 
but  the  lesions  are  more  suppurative  in  character  and  contain  more 
numerous  giant  cells. 

The  lungs  show  discrete,  miliary  to  pea-sized  abscesses  or  confluent 
areas  of  softening.  The  cut  surface  exudes  a  thick,  purulent  fluid 
and  a  soft,  cheesy,  necrotic  material  or  pus  may  be  expressed  from  the 
involved  region.     Ulceration  may  lead  to  cavity  formation.     The 


396 


DISEASES  OF  THE  LUNGS 


lesions   are   prevailingly   bronchopneumonia   in   type.     Microscopic 

examination  shows  in  the  central  parts  of  the  affected  region  an  area 
of  necrosis  containing  blastomycetes,  pus  cells,  red-blood  corpnseles 
and  desquamated  epithelium.  This  central  necrotic  area  is  hounded 
by  a  zone  of  granulation  tissue  in  which  are  giant  cells,  many  or  all 
of  which  may  contain  blastomycetes.  The  peribronchial  lymph  nodes 
may  show  similar  changes.  The  larynx,  trachea  and  bronchi  may  also 
be  involved.    Fibrinous  or  serofibrinous  pleurisy  may  be  present. 


Fig.  60 

SK^ 

Blastomycosis.    Cutaneous  lesions  of  face.     (Fontaine,  Haase,  and  Mitchell.) 

Cutaneous  lesions  are  a  characteristic  feature.  They  comprise 
superficial,  pea-sized  or  larger,  moderately  firm,  subcutaneous  nodules 
which  gradually  enlarge,  soften  and  break  down,  discharging  glairy 
mucopus  and  leading  to  the  formation  of  open  abscesses,  fistulas, 
crusted  or  open  ulcers,  or  scars.  In  Le  Count  and  Myers'1  case  about 
200  cutaneous  lesions  were  present.  Deeper  and  larger  abscesses 
may  be  observed.  At  times  more  typical  cutaneous  manifestations 
are  seen  in  the  form  of  elevated  patches  of  variable  size,  with  a  rough, 
uneven  and  scaling  or  papillomatous  surface  and  with  a  rather  abrupt, 


1  Jour.  Inf.  Dis.,  1907,  vol.  iv. 


PULMONARY  BLASTOMYCOSIS  '      397 

sloping,  dark  red  margin.  Examination,  if  necessary  with  a  hand  lens, 
may  disclose  large  numbers  of  miliary  abscesses  at  the  margin  of  the 
patch. 

In  addition  to  the  cutaneous  and  pulmonary  involvement,  the 
spleen,  kidneys,  liver,  spinal  column,  cerebrum,  cerebellum,  spinal 
cord,  muscles,  bones,  joints,  meninges,  myocardium,  adrenals,  pan- 
creas, colon,  appendix,  prostate  and  lymph  glands  may  be  involved. 
Amyloid  infiltration  has  been  noted. 

Symptoms. — Cutaneous  manifestations  have  usually  preceded  the 
onset  of  pulmonary  symptoms.  In  some  instances  the  history  suggests 
coincident  pulmonary  and  systemic  invasion.  In  a  few  cases  the  initial 
symptoms  have  been  pulmonary.  The  pulmonary  manifestations 
have  usually  been  mild  during  the  early  part  of  the  disease.  There 
may  be  cough,  discomfort  in  the  chest  and  mucopurulent  sputum  at 
times  streaked  or  stained  with  blood.  Laryngitis  with  hoarseness 
or  aphonia  has  been  observed.  On  physical  examination,  the  signs 
are  those  of  consolidation  over  the  more  extensively  involved  regions, 
but  it  has  repeatedly  been  noted  that  at  autopsy  the  pulmonary  lesions 
were  more  extensive  than  the  symptoms  and  signs  seemed  to  indicate 
during  life. 

Fever,  chills,  night  sweats,  loss  of  weight  and  strength  may  also  be 
observed  in  connection  with  pulmonary  and  systemic  involvement. 
Diarrhea,  albumin  and  casts  in  the  urine,  slight  adenopathy,  anemia, 
leukocytosis,  enlargement  of  the  spleen,  arthritis,  caries  of  bone, 
spondylitis  and  corneal  ulceration  and  infection  of  the  vitreous  have 
also  been  observed.    The  ends  of  the  fingers  may  be  clubbed. 

The  course  of  the  disease  is  chronic,  with  exacerbations  and  remis- 
sions. The  clinical  course  is  that  of  pyemia,  Death  is  usually  due 
to  systemic  infection,  but  predominant  pulmonary  invasion  may  be 
largely  responsible  in  a  few  instances.  Following  pulmonary  and 
systemic  invasion  the  disease  usually  terminates  fatally  within  a  few 
months. 

Blastomycetes  have  been  demonstrated  in  the  cutaneous  lesions, 
abscesses,  sputum,  cerebrospinal  fluid,  urine,  feces,  and  blood. 

Diagnosis. — The  disease  should  be  suspected  in  cases  with  pulmonary 
symptoms  associated  with  multiple  abscesses  and  a  clinical  picture 
resembling  pyemia.  In  cases  in  which  the  earliest  manifestations  are 
pulmonary  and  before  the  appearance  of  abscesses  or  the  more  typical 
cutaneous  eruption  the  condition  may  be  mistaken  for  pulmonary 
tuberculosis.  Thus  far  no  case  has  been  reported  running  its  course 
with  a  pulmonary  infection  as  the  sole  manifestation  of  the  disease. 

The  diagnosis  may  be  established  by  recognition  of  the  nature  of  the 
cutaneous  lesions  and  the  demonstration  of  blastomyces  in  pus  from 
the  abscesses  or  in  a  fragment  of  the  tissue.  In  the  investigation  of 
pus,  the  fresh  and  unstained  material  may  be  placed  between  slide 
and  cover-glass  and  a  thin  layer  examined  under  the  microscope. 
The  addition  of  10  per  cent,  sodium  hydrate  to  the  preparation  will 


:\\\s  DISEASES  OF  THE  LUNGS 

bring  out  the  double  contoured  capsule  more  clearly.  Sputum  should 
be  investigated  in  the  same  manner. 

Prognosis. — This  is  unfavorable  for  cases  with  pulmonary  and  sys- 
temic infection.  The  evidence  of  healed  and  healing  pulmonary  lesions 
at  autopsy  in  some  cases  suggests  that  the  disease  is  not  inevitably 
fatal.1 

Prophylaxis. — Prevention  of  mold  growth  in  dwellings  by  proper 
ventilation,  lighting,  and  drainage  may  be  of  importance.2 

Treatment. — This  is  unsatisfactory.  There  is  no  special  therapy. 
Marked  improvement  or  complete  recovery  has  followed  the  use  of 
iodid  of  potash  in  the  cutaneous  form  of  the  disease  and  the  drug 
should  be  tried  in  large  doses  and  over  a  long  period  in  the  systemic 
infection.  Every  effort  should  be  made  to  build  up  the  general  strength 
and  improve  nutrition  by  food,  rest  and,  fresh  air.  The  x-rays  have 
been  successfully  applied  to  small  superficial  lesions.  The  use  of  the 
curette  may  lead  to  dissemination  of  the  organisms.  The  injection 
of  the  filtrate  of  old  cultures  of  blastomycetes  may  prove  of  value.3 

1  Stober.     Arch.  Int.  Med.,  1914,  xiii,  509.  2  Ibid.  3  Ibid. 


CHAPTER  XXIV. 
PULMONARY  ASPERGILLOSIS. 

Under  this  heading  may  be  included  cases  of  pulmonary  infection 
with  one  or  another  species  of  the  genus  Aspergillus.  The  Aspergillus 
fumigatus  is  for  the  most  part  the  species  concerned  in  pulmonary 
infection.  The  fungus  appears  to  be  capable  of  giving  rise  to  inflam- 
matory, suppurative  and  destructive  pulmonary  lesions  as  a  primary 
and  independent  infection,  but  secondary  invasion  of  lungs  already 
the  seat  of  tuberculous  or  other  lesions  is  more  common  in  man. 

Etiology. — The  Organism. — Aspergillus  fumigatus  is  a  fungus  belong- 
ing to  the  family  Perisporeacea.  On  culture  media  it  grows  in  the 
form  of  a  mold,  which  varies  in  color  according  to  the  character  of 
the  media.  Greenish,  bluish  or  gray  colonies  may  be  observed.  The 
growth  is  made  up  of  a  thick  felt-work  of  colorless  septate  tubular 
hyphse  a  few  microns  in  diameter.  Segmentation  is  observed  in  the 
broader,  but  is  absent  in  the  narrower  filaments.  Some  of  the  filaments 
grow  upward  into  the  air  and  produce  at  their  free  extremity  masses 
of  spores.  The  color  of  the  growth  is  due  to  these  spore-bearing 
branches.  The  spores  are  very  small,  round  or  oval,  smooth  and  about 
2.5  to  3.5  microns  in  diameter.  The  spores  are  widely  distributed  in 
the  outer  world,  and  may  be  found  on  vegetable  material  of  various 
kinds,  dust  from  grains,  on  bread,  etc.  They  are  very  resistant, 
especially  against  drying.  Growth  may  be  obtained  on  all  culture 
media  and  is  favored  by  an  abundance  of  moisture  and  oxygen. 
Attempts  to  demonstrate  toxin  production  have  usually  failed,  but 
Bodin  and  Gautier1  report  successful  experiments  in  certain  animals 
by  the  use  of  filtrates  of  cultures.  Curiously  enough  the  pigeon 
proved  resistant  against  the  toxin. 

Intravenous  injection  of  birds  and  animals  with  spores  causes 
death  within  a  few  days,  and  postmortem  examination  shows  lesions 
microscopically  resembling  miliary  tubercles  throughout  the  internal 
organs.  Microscopic  examination  shows  areas  of  suppuration  and 
necrosis  enclosing  the  microorganisms.  Inhalation  experiments 
with  spores  have  given  somewhat  variable  results.  Pigeons  were 
thus  infected  by  Dieulafoy,  Chantemesse  and  Widal2  and  by  Renon.3 
Schutz4  produced  fatal  pneumonia  due  to  aspergillosis  by  inhalation 

1  Ann.  de  l'lnst.  Past.,  1906,  p.  209. 

2  Gaz.  des  Hopitaux,  1890,  p.  821. 

3  Etude  sur  l'aspergillose  chez  les  animaux  et  chez  l'homme,  Paris,  1897,  p.  82. 

4  Mitt.  a.  d.  Kaiserlichen  Gesundheitsamte,  Berlin,  1884,  Bd.  ii,  p.  208. 


4(H) 


DISEASES  OF  THE  LUNGS 


experiments  in  pigeons,  geese,  and  smaller  birds.  Feeding  experiments 
by  Schutz  were  successful  in  a  pigeon.  Mycotic  pneumonia  resulted, 
probably  by  inhalation  of  spores,  and  ended  fatally  on  the  sixteenth 
day.  Renon1  produced  pulmonary  aspergillosis  in  rabbits  fed  on  bran 
containing  spores. 

Fig.  61 


Two  spore-bearing  heads  of  Aspergillus  fumigatus.     (Renon.) 

Aspergillosis  in  Animals. — Infection  by  aspergillus  has  long  been 
recognized  in  birds.  The  first  instance  was  described  in  1815  by  Mayer 
and  Emmert2  who  found  the  fungus  in  the  lungs  of  a  jay.  It  has  since 
been  demonstrated  in  many  different  kinds  of  birds,  infecting  not  only 
the  air  sacs,  bronchial  tubes  and  lungs,  but  also  the  liver,  kidneys,  and 
other  organs.  De  Jong3  describes  an  epidemic  among  canaries  in  a 
part  of  the  Netherlands.  In  many  cases,  a  whitish-yellow  coating 
was  seen  on  the  tongue  and  palate.  In  the  dead  animals  a  similar 
coating  was  found  in  parts  of  the  upper  air  passages.  Yellowish, 
cheesy  nodules  were  present  in  the  lungs.  Involvement  of  the  pleura 
and  peritoneum  in  the  neighborhood  of  the  liver  was  also  noted. 
Aspergillus  fumigatus  and  diplococci  were  isolated  from  the  lesions. 
Cattle,  horses,  swine,  and  other  animals  may  become  infected.  The 
lungs  are  principally  involved  and  the  lesions  resemble  tuberculosis 
or  actinomycosis.  Hellens4  has  described  an  outbreak  of  the  disease 
in  sheep. 

1  Loc.  cit.,  p.  83.  2  Meckel's  Deut.  Arch.,  vol.  i,  p.  310. 

3  Centralis,  f.  Bakt.,  1912,  1  Abt.,  lxvi,  390. 

4  Arb.  a.  d.  path.  Inst.  d.  Universitat.,  Helsingfors,  Berlin,  1905,  Bd.  i,  H.  1-2,  p.  313. 


PULMONARY  ASPERGILLOSIS  401 

Aspergillosis  in  Man. — The  first  report  which  can  he  regarded  as  a 
probable  instance  of  human  infection  with  aspergillus  was  published 
by  Bennett.1  Virchow2  first  determined  the  identity  of  the  parasite 
in  cases  of  pulmonary  infection  in  man.  Dieulafoy,  Chantemesses 
and  Widal3  reported  the  occurrence  of  pulmonary  aspergillosis  in 
three  pigeon  feeders  in  Paris.  The  pigeon  feeders  hold  in  the  mouth 
a  mixture  of  water,  millet  and  vetch  seeds,  which  they  blow  into  the 
mouth  of  the  pigeon.  Several  thousand  pigeons  may  be  thus  fed  in  a 
day.  The  pigeon  feeders  may  become  infected  with  aspergillosis 
from  the  grains  or  through  the  contact  with  infected  birds.  Renon4 
described  the  disease  among  the  hair  sorters  of  Paris  who  are  exposed 
to  an  atmosphere  containing  rye  flour  which  they  use  to  remove  grease 
from  the  hair.  Aspergillus  was  cultivated  from  the  rye  flour,  and  of 
six  pigeons  exposed  to  the  dust  from  this  flour,  five  died  of  aspergillosis, 
the  first  on  the  seventeenth  day  from  the  beginning  of  the  experi- 
ment. 

The  disease  may  be  either  primary  or  secondary.  In  Kohn's5  case 
the  primary  character  of  the  pulmonary  lesions  was  first  established 
by  postmortem  examination.  A  number  of  other  cases  have  since  been 
described,  but  for  the  most  part  the  infection  appears  to  be  engrafted 
on  preexisting  bronchial  or  pulmonary  disturbances. 

Pathology. — The  infected  parts  of  the  lung  show  inflammation, 
suppuration,  and  necrosis.  The  typical  lesion  is  an  area  of  necrosis, 
in  the  centre  of  which  is  a  colony  of  the  fungus.  Such  an  appearance 
may  closely  resemble  actinomycosis.  Close  relation  of  the  involved 
area  to  a  bronchus  may  lead  to  more  marked  growth  of  the  organism 
in  consequence  of  the  favoring  influence  of  an  abundant  supply  of 
oxygen.  Spores  may  then  be  produced  and  lead  to  infection  of  nearby 
or  remote  parts  of  the  lung.  Purulent  liquefaction  is  absent.  The 
necrotic  focus  may  be  sequestrated  and  expelled  with  the  formation 
of  an  odorless  cavity.  Bacterial  invasion  of  the  affected  areas  may 
or  may  not  take  place.  The  usual  absence  of  fetor  may  be  due  to 
inhibition  of  the  growth  of  putrefactive  bacteria  by  the  fungus.  The 
lesions  of  tuberculosis  may  coexist  with  those  due  to  aspergillus.  Pul- 
monary abscess,  gangrene,  bronchiectasis  and  chronic  interstitial 
pneumonia  may  result  from  the  infection.  In  Kockel's6  case  there 
was  a  cavity  the  size  of  an  apple  in  the  left  upper  lobe.  Symptoms 
were  absent  and  the  process  was  apparently  arrested.  In  one  of 
Virchow's7  cases  no  pulmonary  involvement  was  found,  but  several 
large  colonies  of  fungus  in  the  bronchi.    No  significant  changes  in  the 

1  Trans.  Roy.  Soc,  Edinburgh,  1842,  Bd.  xv,  ii,  277. 

2  Beitrage  z.  Lehre  von  den  beim  Menschen  vorkommenden  pflanzlichen  Parasiten, 
Virchow's  Arch.,  1856,  p.  557. 

3  Loc.  cit.  4  Loc.  cit. 
6  Deut.  med.  Woch.,  1893,  No.  50. 

6  Verhandl.  d.  Gesellschaft  d.  Naturf.  u.  Aerzte,  69.  Versamml.  Braunschweig,  1897, 
T.  ii,  H.  2,  p.  19. 

7  Loc.  cit,  p.  569. 

26 


402  DISEASES  OF   THE  LUNGS 

bronchial  mucous  membrane  were  seen  microscopically.  Metastatic 
distribution  of  the  organism  lias  not  been  observed. 

Symptoms. — The  clinical  features  of  primary  aspergillosis  are  those 
of  chronic  pulmonary  tuberculosis  with  cavity  formation  or  chronic 
bronchiolitis  terminating  in  chronic  interstitial  pneumonia.  In  the 
former  type,  there  may  be  cough  with  the  expectoration  of  purulent 
sputum  streaked  with  blood.  More  or  less  abundant  hemoptysis 
may  occur.  As  the  disease  progresses,  digestive  disturbances,  night 
sweats,  evening  elevation  of  temperature  and  emaciation  may  be 
observed.  On  examination,  signs  of  bronchitis,  pulmonary  infiltration 
and  finally  cavity  formation  may  be  established.  The  disease  may  be 
fatal  or  cease  to  progress  and  terminate  in  recovery.  The  indurative 
form  begins  with  symptoms  of  diffuse  bronchitis.  The  cough  is  harass- 
ing and  dyspnea  may  be  a  troublesome  feature.  Evidences  of  emphy- 
sema, pulmonary  induration  and  contraction  become  manifest  as  the 
disease  advances.  As  in  the  preceding  type,  the  termination  may  be 
fatal  with  increasing  marasmus  or  failure  of  the  right  side  of  the  heart. 
Recovery  may  follow.  Pulmonary  tuberculosis  may  complicate  the 
condition.  In  cases  in  which  aspergillosis  is  secondary  to  already  exist- 
ing pulmonary  lesions,  the  clinical  picture  is  lacking  in  distinctive 
features. 

Diagnosis. — This  can  be  made  only  by  the  finding  of  fragments  or 
spores  of  the  fungus  in  the  sputum.  Their  recognition  may  be  facili- 
tated by  the  addition  of  a  20  per  cent,  solution  of  sodium  hydrate  to 
the  specimen  to  dissolve  the  cellular  elements  and  thus  make  the  fungus 
more  clearly  visible.  The  sputum  should  be  fresh,  as  otherwise  sec- 
ondary infection  with  aspergillus  spores  from  the  air  may  take  place. 
Fragments  of  the  fungus  may  be  found  imbedded  in  blood-clots  or 
masses  of  necrotic  pulmonary  tissue.  The  use  of  staining  fluids  is 
superfluous.  Cultivation  of  the  organism  may  be  necessary  to  estab- 
lish the  identity.  For  this  purpose  Paulin's1  fluid  which  has  the 
advantage  of  being  relatively  unfavorable  for  the  growth  of  bacteria 
may  be  used.  The  sputum  is  added  to  50  c.c.  of  the  sterile  solution 
in  a  100  c.c.  flask.  Aspergillus  fumigatus  colonies  develop  at  a 
temperature  of  38°  to  40°  in  three  to  four  days.  Evidences  of 
pulmonary  destructive  lesions  without  foul  odor  to  the  sputum, 
especially  in  persons  engaged  in  occupations  likely  to  lead  to  the 
inhalation  of  aspergillus  spores,  should  suggest  the  possibility  of 
the  disease.  Actinomyces  and  tubercle  bacillus  should  also  be  sought 
in  the  sputum. 

Prognosis. — This  is  uncertain,  but  on  the  whole  not  promising  for 
complete  recovery  since  even  in  the  uncommon  instances  in  which 
the  aspergillus  infection  comes  to  a  standstill,  the  damage  to  the  lung 
is  persistent,  and  may  finally  lead  to  a  fatal  termination.  Pulmonary 
tuberculosis  may  be  engrafted  on  the  aspergillus  infection.    The  slow 

J  Set-  Sticker,  Nothnagel's  spec.  Path.  u.  Ther.,  1900,  1  Abth.,  Bd.  ii,  vol.  xiv. 


PULMONARY  ASPERGILLOSIS  403 

course  and  absence  of  generalization  of  the  organism  throughout  the 
body  make  the  prognosis  of  the  primary  form  less  grave  than  in  pul- 
monary tuberculosis.  The  outlook  in  the  cases  with  symptoms  of 
chronic  bronchiolitis  and  emphysema  seems  somewhat  less  favorable 
than  in  those  resembling  pulmonary  tuberculosis. 

Prophylaxis. — Means  should  be  taken  to  prevent  the  inhalation  of 
dust  containing  aspergillus  spores  in  occupations  involving  this  danger 
by  cleanliness,  proper  ventilation,  and  if  necessary,  the  use  of  respira- 
tors. Persons  already  subject  to  pulmonary  disturbances  are  probably 
more  susceptible  to  infection  with  aspergillus  and  should  be  especially 
careful  to  avoid  exposure. 

Treatment. — Any  further  chance  for  infection  must  be  prevented 
by  avoidance  of  contact  with  dry  grains  and  vegetable  material. 
There  is  no  specific  therapy.  Chief  reliance  must  be  placed  on  improve- 
ment of  the  general  strength  and  nutrition,  by  an  abundance  of  good 
food  and  fresh  air  free  from  dust.  Measures  similar  to  those  recom- 
mended for  pulmonary  tuberculosis  may  be  applied  with  advantage 
to  the  treatment  of  this  disease.  The  internal  administration  of  iodid 
of  potash,  or  arsenic  in  the  form  of  Fowler's  solution  may  be  tried. 


CHAPTER   XXV. 
ANIMAL  PARASITES. 

ECHINOCOCCUS  DISEASE  OF  THE  LUNG. 

Etiology. — Sources  of  Infection. — Dogs  used  for  herding  sheep  are 
the  usual  source.  A  small  tapeworm,  Tenia  echinococcus,  inhabits 
the  small  intestine  of  the  dog  and  may  occur  also  in  other  animals 
such  as  the  wolf,  jackal,  canis  dingo  (Australian  wild  dog),  and  the 
cat.  Echinococcus  disease  is  the  larval  stage  in  the  life  cycle  of  the 
parasite  and  occurs  in  a  large  number  of  domesticated  and  some  wild 
animals.  Sheep,  cattle  and  swine  are  the  most  frequent  and  important 
intermediate  hosts.  The  infection  of  man  is  accidental  and  relatively 
uncommon. 

Incidence  of  the  Pulmonary  Disease. — This  appears  to  be  second  in 
importance  to  the  disease  in  the  liver,  which  embraces  from  50  per 
cent.  (Neisser)  to  69  per  cent.  (Finsen)  of  all  cases.  Among  Neisser's1 
983  cases,  only  67  (6.8  per  cent.)  were  pulmonary.  Bezou2  found  153 
(8.2  per  cent.)  pulmonary  hydatids  among  1852  cases.3  Vegas  and 
Cranwell4  report  54  (5.6  per  cent.)  among  952  cases,  collected  in  Buenos- 
Ay  res  and  Rosario. 

The  sexes  are  about  equally  affected.  The  disease  may  occur  at 
any  age,  but  more  often  from  twenty  to  forty  years.  It  is  more  com- 
monly seen  among  the  poorer  classes  and  those  living  in  close  contact 
with  dogs. 

Pathogenesis. — The  eggs  of  the  Tenia  echinococcus  are  eliminated 
with  the  dog's  feces  in  the  terminal  ripe  segment  of  the  worm  and  may 
be  ingested  with  contaminated  food  or  drinking  water.  They  may 
also  be  carried  to  the  mouth  on  hands  soiled  in  petting  dogs.  The 
embryo,  liberated  from  its  shell  in  the  stomach,  bores  its  way  by  means 
of  its  armature  of  six  hooks  to  various  parts  of  the  body. 

(A)  Pulmonary  Echinococcus. — Primary  Echinococcus  of  the  Lung.— 
This  is  the  most  common  form.  The  path  taken  by  the  embryo  is 
not  clear.  Migration  by  way  of  the  portal  blood-stream,  thence  through 
the  diaphragm  and  pleura,  is  suggested  by  the  greater  frequency  of 
echinococcus  of  the  liver  and  the  right  lobe  of  the  lung.    As  the  disease 

1  Die  Echinococcuskrankheit,  1877,  p.  25. 

2  Etudes  sur  les  kystes  hydatiques  du  poumon  Paris,  1893. 

3  Combined  Statistics  of  Davaine,  Cobbolt,  Neisser,  and  Finsen. 
*  Rev.  de  Chir.,  1901,  xxiii,  970. 


ECHINOCOCCUS  DISEASE  OF  THE  LUNG  405 

may  be  round  not  only  in  other  parts  of  the  lung  but  in  any  region 
of  the  body,  this  is  probably  not  the  only  route  which  the  embryo  run 
follow. 

Bird1  suggested  that  the  eggs  of  the  Tenia  echinococcus,  deposited 
with  the  feces,  may  be  distributed  as  dust  and  gain  entrance  to  the 
lungs  by  inhalation,  thus  giving  rise  to  pulmonary  invasion.  There 
is  no  proof  of  such  a  path  of  infection  and  the  preponderance  of  cases 
with  hepatic  involvement  is  against  it. 

The  development  of  the  disease  in  the  lung  does  not  differ  from  that 
in  other  regions  of  the  body.  The  embryo  gradually  increases  in  size 
and  presents  an  outer,  thick,  elastic  cuticle,  at  first  homogenous, 
later  laminated,  and  an  inner  parenchymatous  or  germinal  layer. 
This  inner  layer  surrounds  a  cavity  containing  fluid.  Brood  capsules, 
in  which  heads  (scolices)  form,  develop  from  the  parenchymatous 
layer.  Further  growth  may  lead  to  the  formation  within  the  parent 
cyst  of  daughter  and  granddaughter  cysts  (endogenous  echinococcus). 
This  is  the  form  usually  found.  I  have  not  seen  that  form  in  which 
growth  takes  place  by  external  budding  (exogenous  echinococcus) 
reported  for  the  lung,  although  it  probably  occurs.  In  rare  instances, 
as  in  the  case  reported  by  Hauser,2  the  echinococcus  multilocularis  has 
been  found  in  the  lung. 

Secondary  Echinococcus  of  the  Lung. — This  is  less  common  than  the 
primary  form,  (a)  By  Extension.  It  is  possible  that  from  pulmonary 
hydatids,  by  the  process  of  external  budding  above  mentioned,  small 
cysts  may  find  their  way  through  the  bronchi  to  remote  parts  of  the 
lung  and  there  continue  to  grow.  A  similar  implantation  of  small 
cysts  after  spontaneous  or  artificial  rupture  into  the  lung  of  a  parent 
cyst  in  the  parapulmonary  tissues  is  also  possible  as  in  the  develop- 
ment of  peritoneal  cysts  after  rupture  of  an  intra-abdominal  echino- 
coccus. This  method  of  origin  receives  some  confirmation  in  the  experi- 
ments of  Deve.3  Three  rabbits  were  inoculated  intratracheally  with 
fluid  obtained  from  the  hydatid  of  the  sheep.  One  animal  died  after 
fifty-one,  the  others  were  killed  after  fifty-seven  days.  Investigation  of 
the  lungs  showed  numerous  white  miliary  granulations,  some  of  which 
represented  small  cysts.  Microscopic  examination  showed  cyst  for- 
mation, a  stratified  cuticle  and  an  inner  parenchymatous  layer.  Serial 
sections  demonstrated  a  mass  of  hooklets  in  the  wall  of  each  vesicle. 
Secondary  infection  of  the  parent  cyst  with  bacteria  usually  precedes  or 
so  quickly  follows  rupture  that  spread  of  the  parasite  by  this  means  is 
not  likely  to  be  of  frequent  occurrence. 

(b)  By  Metastasis. — It  is  probable  that  multiple  and  isolated  cysts 
in  various  parts  of  the  body  are  usually  due  to  infection  with  more 
than  one  embryo  of  the  Tenia  echinococcus  at  the  same  or  at  different 

1  On  Hydatids  of  the  Lungs,  Melbourne  and  Sydney,  1877. 

2  Primar,  Echin.  multilocularis  der  Pleura  u.  d.  Lunge,  Erlangen  u.  Leipzig,  1901. 

3  Encemencement  intratracheal  de  sable  echinococcique,  Echinococose  secondaire  du 
poumon  d'origine  bronchique,  Mem.  de  la  Soc.  de  Biol.,  1904,  vol.  lvii. 


406  DISEASES  OF   THE  LUNGS 

times.  An  exception  must  be  noted  for  the  echinococcus  multilocularis, 
in  which  the  parenchymatous,  germinal  layer  exists  both  on  the  inner 
and  outer  side  of  the  chitinous  cuticle.  From  the  outer  germinal 
layer,  ameboid  embryos  are  produced  and  may  infect  not  only  the 
immediate  neighborhood  of  the  primary  growth  but  also  more  remote 
regions  by  entrance  into  the  blood  or  lymphatic  vessels. 

Pulmonary  embolism  following  rupture  and  evacuation  of  cysts  into 
the  larger  venous  channels  is  not  known  to  have  given  rise  to  the  implan- 
tation and  further  development  of  the  parasite,  but  has  been  recorded 
in  rare  instances  as  a  cause  of  death.  Twelve  cases  have  been  collected 
to  1905  by  Gamier  and  Jornier1  who  add  a  thirteenth  case  of  their  own. 
The  embolism  was  secondary  to  rupture  of  cysts  of  the  liver,  with 
evacuation  of  membrane  or  daughter  cysts  into  the  vena  cava,  or  of 
cysts  of  the  heart  breaking  into  the  right  auricle  or  ventricle.  The 
symptoms  do  not  differ  from  those  following  pulmonary  embolism 
from  other  causes.  Occlusion  of  the  main  trunk  or  one  of  the  principal 
branches  of  the  pulmonary  artery  is  usually  followed  by  death  within 
a  few  minutes  or  hours.  After  invasion  of  smaller  branches,  life  may 
be  prolonged  for  weeks. 

(B)  Parapulmonary  Echinococcus. — (a)  Intact  Cysts. — In  this  group 
may  be  included  cysts  of  neighboring  regions  which  in  their  growth 
encroach  upon  the  pulmonary  space.  It  is  not  infrequent  for  hepatic 
cysts  to  grow  upward,  pushing  the  diaphragm  before  them.  They 
may  reach  as  high  as  the  second  rib  or  the  clavicle.  Subdiaphragmatic 
cysts  developing  in  the  region  between  the  liver  and  diaphragm,  in 
the  spleen  or  kidney,  may  likewise  elevate  the  diaphragm  without 
actually  invading  the  lung.  The  condition  of  the  pleura  has  an  impor- 
tant bearing  on  the  subsequent  course  of  cysts  growing  in  its  neighbor- 
hood. It  may  be  free  or  inflamed  and  the  site  of  serous,  serofibrinous  or 
purulent  exudate.  Partial  or  complete  pleural  adhesion  is  more  com- 
mon, however,  and  in  this  case,  widespread  pleural  infection  is  avoided 
following  the  rupture  of  the  cyst. 

(b)  Perforated  Cysts. — According  to  Neisser's  statistics,  hepatic 
cysts  rupture  into  the  respiratory  apparatus  in  about  11  per  cent, 
of  the  cases.  Suppuration  of  the  cysts  almost  constantly  precedes 
the  rupture.  Evacuation  into  the  lung  or  bronchi  is  more  common 
than  into  the  pleura.  In  Neisser's  60  cases,  the  pleura  was  invaded 
in  16,  the  lungs  or  bronchi  in  44.  Hepatopleural  or  hepatobronchial 
fistula3  may  result.  Bile  may  be  found  in  the  pleural  cavity  or  be 
expectorated. 

Pathology. — The  cysts  may  be  found  at  any  part  of  the  lung,  but 
the  right  side  and  especially  the  right  lower  lobe  is  most  often  affected. 
In  Neisser's  statistics,  the  right  side  was  involved  in  25,  the  left  in 
only  12  instances.  The  disease  was  present  on  both  sides  in  6.  Coin- 
cident disease  of  the  lungs  and  other  organs  is  frequent.     Multiple 

1  La  Presse  med.,  Paris,  1905,  i,  369-371. 


ECHINOCOCCUS  DISEASE  OF  THE  LUNG  107 

infections  usually  involve  the  liver  and  the  lung.  The  pulmonary 
cysts  vary  in  size  from  that  of  a  pea  to  a  child's  head. 

An  important  feature  of  the  cysts  is  the  presence  outside  the  thick, 
elastic  cuticle  of  the  parasite  itself  of  an  adventitious  membrane  or 
connective-tissue  capsule  which  separates  the  cyst  from  the  pulmonary 
parenchyma.  This  capsule  is  usually  thin.  Its  inner  surface  is  smooth 
and  is  bounded  externally  by  healthy  lung  tissue.  In  some  instances, 
it  is  thick.  Large,  old  cysts,  which  have  ruptured,  may  be  surrounded 
by  a  dense  leathery  capsule,  about  which  the  lung  shows  chronic- 
interstitial  changes  of  varying  extent.  The  capsule  is  not  invariably 
present  and  some  small  cysts  appear  to  lie  in  direct  contact  with 
healthy  pulmonary  tissue.  The  bronchi  may  terminate  in  the  wall  of 
the  capsule,  by  larger  or  smaller  openings,  thus  presenting  free 
communications  between  the  cavity  and  the  air-passages  and  favoring 
the  entrance  of  bacteria  into  the  sac  or  the  exit  of  cystic  fluid  in 
case  of  rupture. 

Perforation  of  the  cyst  is  common.  Rupture  leads  to  evacuation  of 
the  contents  into  the  region  between  the  cyst  membrane  and  the  adven- 
titious capsule  from  which  it  usually  escapes  into  the  bronchi.  Perfora- 
tion may  also  occur  into  the  pleural  cavity.  Depending  on  the  previous 
condition  of  the  pleura,  and  the  character  of  the  cyst  contents,  this  is 
followed  by  an  accumulation  within  the  pleura  of  free  or  encysted 
cystic,  serous,  or  purulent  fluid.  Evacuation  into  the  pleura  is  likely 
to  be  followed  by  the  escape  of  cystic  fluid  by  the  bronchi  and  the 
admission  of  air  into  the  pleural  cavity,  with  the  formation  of  pneu- 
mothorax. If  the  pleura  is  obliterated  before  rupture  occurs,  pul- 
monary echinococcus  may  perforate  externally.  In  rare  instances, 
perforation  may  take  place  into  the  spinal  canal,  the  pericardium, 
the  intestines,  or  the  peritoneum. 

Suppuration  of  the  cyst  may  precede  or  follow  rupture.  The  con- 
tents is  converted  into  an  abscess.  Inflammation  of  the  neighboring 
pulmonary  tissue  takes  place.  Pulmonary  gangrene  may  be  a  conse- 
quence. Thrombosis  of  pulmonary  veins  may  be  induced.  Erosion 
of  pulmonary  vessels  may  result  in  severe  or  even  fatal  hemorrhage. 
Pulmonary  embolism  following  the  entrance  of  daughter  cysts  into 
eroded  vessels  has  been  observed.  Pulmonary  tuberculosis  occasionally 
complicates  the  process.  Long  continued  suppuration  may  lead  to 
chronic  interstitial  changes  in  the  surrounding  tissue.  In  favorable 
cases,  the  fluid  contents  of  the  cyst,  daughter  cysts  and  the  cyst 
membrane  are  expectorated.  The  cavity  gradually  diminishes  in  size 
and  small  losses  of  substance  may  completely  cicatrize. 

Symptoms  and  Signs. — In  the  early  stage  of  the  development  of 
the  disease  there  are  usually  no  symptoms.  This  latent  interval  is  of 
variable  duration  and  may  last  for  weeks,  months  or  years,  It  is 
more  likely  to  be  short  when  the  pleura  is  involved  or  the  cyst  becomes 
infected  early  in  its  growth.  Central  and  uninflamed  cysts  usually 
present  the  longest  latent  interval. 


408  DISEASES  OF  THE  LUNGS 

The  initial  disturbances  arc  usually  cough,  hemoptysis,  dyspnea 
and  pain  or  a  sense  of  thoracic  oppression.  In  a  small  proportion  of 
the  cases,  the  onset  is  sudden  with  hemoptysis,  the  expectoration  of 
cystic  fluid,  cysts  or  membrane,  or  severe  dyspnea  following  rupture 
into  the  pleura  and  pneumothorax.  In  rare  instances,  such  cases  are 
immediately  fatal  from  hemorrhage  or  suffocation.  The  different 
symptoms  may  be  more  fully  considered. 

The  cough  is  usually  dry  in  the  early  course  of  the  disease  and  may 
be  unaccompanied  by  expectoration  until  rupture  takes  place.  It 
may  be  constant,  but  is  more  often  paroxysmal.  Sputum  if  present 
is  usually  scanty  and  due  to  an  accompanying  bronchitis. 

Hemoptysis  is  an  important  and  early  symptom.  It  is  absent  only 
in  rare  instances;  is  usually  preceded  by  cough,  but  may  be  the  first 
indication  of  the  disease.  Preceding  rupture,  the  bleeding  is  seldom 
abundant  and  is  likely  to  consist  of  bloody  streaks  or  small  amounts  of 
fresh  blood  in  the  expectoration.  Such  hemorrhages  probably  come 
from  slight  erosions  of  the  connective-tissue  capsule  or  the  neighboring 
lung.  The  bleeding  is  usually  repeated,  the  attacks  coming  at  varying 
periods,  with  freedom  from  hemorrhage  during  the  intervals.  The 
patient's  general  condition  is  undisturbed  and  there  is  usually  no  fever. 
Abundant  and  even  alarming  hemorrhages  occasionally  occur  during 
the  early  stages  of  the  disease,  as  in  Kiiss'1  case,  in  which  an  hemoptysis 
of  about  a  quart  is  said  to  have  preceded  by  over  two  years  a  second 
attack  followed  by  the  expectoration  of  a  large  amount  of  glairy, 
fetid  fluid.  Hemoptysis  accompanying  or  following  rupture  may  be 
due  to  erosion  of  the  larger  branches  of  the  pulmonary  vessels  and  is 
occasionally  fatal. 

The  dyspnea  is  slowly  progressive  and  in  the  absence  of  complica- 
tions its  degree  depends  on  the  amount  of  pulmonary  space  occupied 
by  the  cyst.  It  may  be  intermittent.  Aggravation  of  the  dyspnea 
may  be  coincident  with  attacks  of  bronchitis.  A  sensation  of  weight, 
fulness  and  discomfort  in  the  affected  part  of  the  lung  is  not  infre- 
quent. Pain  is  common  but  is  not  usually  an  urgent  symptom  unless 
the  pleura  is  inflamed.  The  disease  is  afebrile.  The  general  health 
is  little  if  at  all  disturbed.  Dysphagia  has  not  been  observed  with 
pulmonary  echinococcus.  In  rare  instances,  the  pupils  are  unequal. 
Clubbing  of  the  ends  of  the  fingers  and  incurvation  of  the  nails  (Hippo- 
cratic  fingers)  have  been  seen.  This  condition  may  gradually  disappear 
after  the  evacuation  of  the  cysts,  as  in  Frobeen's2  case.  The  jugular 
veins  may  be  dilated.  Edema  confined  to  the  upper  extremities  was 
observed  by  Leroux.3  Edema  of  the  lower  extremities  is  at  times  seen 
in  the  later  stages  of  the  disease.  Weakness  or  hoarseness  of  the  voice 
is  sometimes  present.    Aphonia  has  not  been  noted. 

With  small  cysts,  centrally  placed,  there  may  be  no  physical  signs. 

1  Societe  anatomiquc  de  Paris,  1907,  p.  494. 

2  St.  Petersburger  med.  Woch.,  1903,  N.  F.  xx,  p.  94. 

3  See  Hearn,  Kystes  Hydatiques  du  poumon  et  de  la  plevrc,  p.  115. 


ECHINOCOCCUS  DISEASE  OF  THE  LUNG  10!) 

In  the  presence  of  larger  unruptured  cysts,  the  inspiratory  excursion 
of  the  affected  side  is  likely  to  be  diminished.  The  chest  wall  oxer- 
lying  the  growth  occasionally  shows  a  local  prominence,  and  the  cor- 
responding side  may  be  larger  by  measurement.  The  diaphragm 
shadow,  below  the  involved  region,  may  be  present,  but  of  diminished 
amplitude.  The  affected  area  is  dull  or  flat,  but  the  transition  from 
dulness  or  flatness  to  normal  pulmonary  resonance  may  be  more  abrupt 
than  with  pleural  effusion.  Shifting  dulness  is  not  observed.  Hydatid 
fremitus  is  not  recorded  for  the  pulmonary  form.  The  upper  limit 
of  a  mass  at  the  base,  marked  out  by  percussion,  is  not  likely  to  show 
such  a  curve  as  is  present  with  free  pleural  fluid,  but  is  more  often 
rounded,  with  a  convex  upper  margin,  and  may  then  resemble  encysted 
pleural  exudate.  At  times,  a  zone  of  resonance  may  separate  its  lower 
limit  from  the  base  of  the  lung.  Tactile  fremitus  is  usually  absent. 
The  sound  of  the  spoken  voice  and  whisper  is  diminished  or  inaudible. 
The  respiratory  murmur  is  feeble  or  lost.  A  sudden  transition  to  nor- 
mal or  exaggerated  breathing  may  be  noted  at  the  periphery  of  the 
involved  region.  This  is  due  to  pulmonary  compression.  Rales  are 
not  heard,  unless  the  case  is  complicated.  Displacement  of  the  heart 
to  the  side  away  from  the  cyst  and  of  the  liver  or  spleen  dowmward 
may  also  be  noted.  Coincident  inflammation  of  the  lung  or  pleura 
may  mask  or  vary  the  physical  signs. 

Preceding  rupture,  there  are  usually  no  distinctive  symptoms  or 
signs.  Perforation  of  the  cyst  is  commonly  the  first  positive  indication 
of  the  disease.  It  may  occur  spontaneously,  or  follow  inflammation, 
trauma,  exertion  or  puncture.  Cough  and  dyspnea  are  frequent  initial 
symptoms.  Hemoptysis  may  precede  or  accompany  the  attack. 
The  evacuation  of  the  cyst  contents  is  more  often  into  the  bronchi, 
but  the  pleura  may  be  alone  or  coincidently  invaded.  Rupture  into 
other  regions  is  infrequent.  Discharge  by  the  bronchi  may  be  accom- 
panied by  urgent  symptoms  of  suffocation.  Severe  pain  may  follow 
pleural  involvement.  Expectorated  fluid  is  seldom  clear  and  watery. 
It  is  often  mixed  with  pus  or  blood  and  may  contain  cysts  or  cyst 
membrane.  It  may  be  fetid  from  disintegration  of  the  contents  of 
the  cyst  or  the  neighboring  lung.  A  salty  taste  may  be  noted  by  the 
patient.  Death  from  hemorrhage,  flooding  of  the  respiratory  tract 
with  fluid,  or  impaction  in  the  air  passages  of  cysts  or  cyst  mem- 
brane may  follow  the  rupture. 

When  the  fluid  is  unmixed  with  blood  or  pus,  it  is  clear,  watery  and  of 
a  specific  gravity  of  1009  to  1012.  Sodium  chloride  is  present.  Albumin 
may  be  absent  or  present  only  in  small  amounts.  Traces  of  inosit, 
succinic  acid  and  grape  sugar  may  be  found,  but  are  not  distinctive 
features.  At  times,  especially  in  old  cysts,  cholesterin  crystals  are 
present.  Cholesterin  crystals  have  been  found  in  pulmonary  hydatid 
fluid,  among  others  by  v.  Jaksch.1    In  suspected  cases,  cysts  and  bits 

1  Klinische  Diagnostik,  1887,  p.  79. 


410 


DISEASES   OF   THE   Ll'XGS 


of  membrane  should  be  carefully  sought.  The  latter  lias  a  character- 
istic lamellated  structure.  The  sediment  should  be  examined  micro- 
scopically for  scolices  and  hooklets.  These  may  be  found  only  after 
long  search.  Elastic  tissue  may  be  present,  if  pulmonary  destruction 
is  taking  place. 

Fig.  62 


Echinococcus  scolices. 
Fig.  63 


/* 

"%r£ 

Echinococcus  scolicei 


Hepatic  cysts  which  rupture  through  the  lung  usually  lead  to  the 
expectoration  of  ochre-yellow,  bile-stained  sputum.  Positive  tests 
for  bile  pigments  may  be  obtained.    Bilirubin,  cholesterin,  and  hem  a- 


ECHINOCOCCUS  DISEASE  OF   THE  LUNG  411 

toidirf  crystals  may  be  found.  Perforation  of  the  lung  by  cysts  of  the 
liver  has  been  reported  by  Neisser,1  Von  Leyden,2  Guttmann,3  Lenhartz,4 
and  Auerbach.5  As  the  cyst  may  be  walled  off  from  the  biliary  pas- 
sages, bile  in  the  sputum  is  not  a  necessary  feature.  Cholesterin 
crystals  occur  in  the  sputum  not  only  with  echinococcus  cysts,  but 
also  occasionally  with  pulmonary  tuberculosis  and  following  the 
perforation  into  the  lung  of  old  empyema  or  hemorrhagic  pleural 
effusions.  When  they  are  found  in  the  sputum,  however,  it  is  well  to 
have  echinococcus  disease  in  mind. 

Fig.  64 


Echinococcus  hooklets.      X  375. 

Urticaria  is  frequently  observed  after  rupture  of  cysts  into  the  serous 
membranes  and  occasionally  after  evacuation  into  the  bronchi.  Its 
occurrence  in  patients  with  pulmonary  symptoms  should  suggest  the 
possibility  of  this  disease.  A  characteristic  expectoration  may  be 
lacking,  but  a  careful  search  of  the  expectorated  material  may  make  the 
diagnosis  clear.  Dieulafoy6  reports  the  case  of  a  man,  aged  forty  years, 
with  hemoptysis,  frequent  attacks  of  nocturnal  oppression  and  dyspnea 
for  a  period  of  four  months.  This  was  regarded  as  asthmatic  in  origin. 
During  an  attack,  the  expectoration  of  an  abundant  purulent  sputum 
was  followed  by  severe  urticaria,  suggesting  the  possibility  of  hydatid 
disease.  Careful  investigation  of  the  sputum  then  led  to  the  finding 
of  hooklets. 

After  rupture  of  the  cyst,  evacuation  may  rapidly  or  slowly  take 
place.  It  is  not  uncommon  for  daughter  cysts  or  cyst  membrane  to  be 
evacuated  at  intervals  over  a  considerable  period.  Fever,  sweats  and 
loss  of  weight  and  strength  are  common  at  this  stage  of  the  disease, 

1  Die  Echinococcuskrankheit,  Berlin,  1877. 

2  Deut.  med.  Woch.,  1885,  p.  44,  u.  76. 

3  Verhandl.  des  Vereins  f.  innere  Med.,  1884-85,  p.  184  u.  193. 

4  Berl.  klin.  Woch.,  1899,  p.  555.  5  Deut.  Aerzte  Zeit.,  1901,  iii,  533. 

6  Quoted  from  Frankel  Spezielle  Path.  u.  Therap.  d.  Lungenkrankheiten,  1904,  p.  922. 


412  DISEASES  OF   THE  LUNGS 

owing  to  almost  constant  suppuration.  Kales  arc  almost  invariably 
present  over  the  invoked  region  or  a  wider  area.  The  signs  of  cavity, 
tympany  on  percussion,  cracked  pot  resonance,  a  variation  in  the  per- 
cussion sound  with  the  mouth  open  and  closed,  and  on  changing  the 
position  of  the  patient,  bronchial  and  amphoric  breathing,  metallic 
tinkle  and  metallic  rales  may  be  present.  Foul,  purulent  sputum, 
containing  clastic  tissue  or  shreds  of  pulmonary  substance  may  indi- 
cate the  existence  of  pulmonary  gangrene.  If  the  pleura  has  been 
invaded,  pleural  friction  may  be  heard  or  the  presence  of  empyema 
or  pyopneumothorax  may  be  established.  In  unfavorable  cases,  the 
course  of  the  disease  is  progressively  downward.  If  evacuation  of  the 
suppurating  cavity  is  not  accomplished  spontaneously  or  by  operation, 
the  patient  may  succumb  with  symptoms  of  sepsis.  Multiple  pul- 
monary abscesses,  arising  by  extension  or  aspiration  of  infected  mate- 
rial into  neighboring  parts  of  the  lungs,  are  likely  to  be  followed  by 
long-continued  pulmonary  suppuration.  Interstitial  pneumonia  may 
accompany  these  changes.  The  occasional  coexistence  of  pulmonary 
tuberculosis  and  echinococcus  disease  of  the  lung  should  be  remembered 
and  the  sputum  frequently  examined  for  tubercle  bacilli. 

Blood. — An  eosinophilia  in  the  circulating  blood  is  frequently  found. 
Of  over  30  cases  of  hydatid  disease  collected  by  Cabot1  only  two  were 
negative.  The  eosinophilia  may  amount  to  as  high  as  40  per  cent.,2 
57  per  cent.,3  or  68  per  cent.,4  but  smaller  percentages  are  more  common. 
The  absence  of  eosinophilia  has  been  recorded  by  Bezancon  and  Weil.5 
Gourand,6  Chauffard  and  Boidin,7  and  Boidin  and  Fiessinger.8  Echino- 
coccus disease  is  only  one  of  many  conditions  giving  rise  to  eosinophilia. 

Duration. — This  is  very  variable.  Owing  to  the  usual  absence  of 
symptoms  in  the  early  development  of  pulmonary  hydatids,  the  date 
of  onset  is  impossible  to  determine  in  most  cases.  To  judge  from  the 
growth  in  accessible  regions,  it  may  take  from  six  months  to  a  year 
to  reach  the  size  of  the  fist.  Symptoms  may  not  be  noted  until  the 
mass  is  considerably  larger  than  this,  and  it  is  probable  that  in  some 
cases  many  years  may  elapse  during  which  the  cyst  is  latent.  Then 
follows  a  period  of  symptoms  such  as  have  been  described,  and  this 
interval  may  occupy  from  a  few  weeks  to  five,  six  or  more  years.  In 
favorable  instances,  rupture  is  followed  by  recovery.  Convalescence 
may,  however,  be  slow  and  repeated  partial  evacuation  may  extend 
over  several  years.  In  some  cases,  the  patient  is  left  with  a  chronic 
pulmonary  infection  from  which  he  never  completely  recovers. 

Diagnosis. — A  history  of  opportunity  for  contagion  is  of  impor- 
tance. Echinococcus  disease  occurs  only  in  rare  instances  in  North 
America  and  Great  Britain,  and  then  almost  always  in  foreigners.    As 

1  Clinical  Examination  of  the  Blood,  1904,  5th  ed. 

2  Achard  and  Clerc,  Ref.  in  Arch.  Gen.  de  Med.,  1902,  p.  743. 

3  Seligmann  and  Dudgeon,  Lancet,  June  21,  1902. 

•'  Palazzo,  Giorn.  Internazione  de  la  Mediche,  Bd.  xxxi. 

6  Arch.  Gen.  de  Med.,  1902,  p.  743.  c  Soc.  Anatom.,  January  10,  1900. 

7  Soc.  raed.  dea  hop.,  December  13,  1907.  s  Ibid.,  January  31,  1908. 


ECHIN0C0CCU8  DISEASE  OF  THE  LUNG  U3 

Stiles  observes,  the  parasite  is  part  of  our  American  fauna.  Infection 
of  man  is  therefore  possible  from  indigenous  sources.  Previous  resi- 
dence where  the  disease  is  prevalent  and  contact  with  dogs  which  are 
or  have  been  used  for  herding  sheep  is  significant. 

The  history  of  an  insidious  onset  and  latent  course  of  a  pulmonary 
affection  which  gives  rise  to  the  signs  of  pleural  effusion  elsewhere 
than  at  the  base  of  the  lung  is  suggestive.  If  at  the  base  a  rounded, 
convex  upper  border,  a  zone  of  pulmonary  resonance  below,  persis- 
tence of  the  diaphragm  shadow  on  the  affected  side,  abrupt  transition 
from  dulness  to  resonance  and  from  diminished  or  absent  to  normal 
or  exaggerated  breathing  may  also  be  of  value.  Physical  signs  of 
extensive  pulmonary  disease  running  an  afebrile  course  in  a  well- 
nourished  individual  or  an  eosinophilia  in  the  circulating  blood  may 
be  factors  of  moment  in  suggesting  the  condition.  The  discovery  of 
an  hydatid  cyst  elsewhere,  as  in  the  liver,  may  also  serve  to  explain 
an  otherwise  obscure  pulmonary  affection. 

It  is  important,  if  possible,  to  make  the  diagnosis  before  rupture 
occurs  and  without  resort  to  thoracentesis.  Serum  diagnosis  by  the 
method  of  complement-fixation  now  offers  the  hope  that  this  may  be 
done.  A  history  of  cough  with  the  expectoration  of  clear,  watery 
fluid,  of  bits  of  membrane  or  of  blood  followed  by  urticaria  is  im- 
portant evidence.  Rupture  of  the  cyst  is  not  always  obvious  and  a 
careful  search  should  be  made  for  scolices,  hooklets,  cysts,  or  cyst 
membrane  in  the  expectoration. 

X-ray  Examination. — When  possible  this  should  always  be  done. 
An  earlier  diagnosis  may  be  possible  by  this  means  than  by  any  other 
method  of  investigation.  Important  evidence  may  be  obtained  con- 
cerning the  size  and  position  of  the  growth.  It  may  result  also  in  the 
discovery  of  multiple  cysts,  only  one  of  which  has  been  suspected. 
Plates  are  more  satisfactory  than  the  fluoroscopic  screen.  The  ex- 
posure is  best  made  while  the  breath  is  held  in  full  inspiration,  during 
which  the  chest  is  bigger  and  the  relation  of  the  tumor  to  the  dia- 
phragm is  better  defined,  owing  to  the  absence  of  blurring  from  res- 
piratory motion.  Intact  cysts  appear  on  the  plate  as  shadows  of  a 
uniform  density,  sharply  limited  from  the  neighboring  lung  and  of 
a  rounded  contour.  In  some  cases  a  zone  of  normal  pulmonary  tissue 
may  intervene  between  the  growth  and  the  diaphragm  below.  Such 
an  observation,  together  with  the  clinical  features  of  the  case,  may 
confirm  the  suspicion  of  echinococcus  disease.  Perforated  cysts 
may  be  indicated  by  a  sharply  limited,  rounded  shadow,  with  a  rela- 
tively clear  centre.  In  the  case  described  by  Levy,  Dorn  and  Zadek.1 
the  patient,  aged  forty  years,  expectorated  echinococcus  membrane 
one  year  after  an  initial  hemoptysis.  Physical  examination  showed 
no  dulness,  but  occasional  rales  over  the  right  lower  lobe.  X-ray 
examination  disclosed  a  shadow  at  the  base  of  the  right  lung,  5  by 

1  Verhandl.  d.  Berliner  med.  Gesellsch.,  1899,  xxx,  170. 


414 


DISEASE'S  OF   THE  LUNGS 


4  cm.,  with  a  dark  border  and  a  clear  centre.  This  was  interpreted 
as  a  ruptured  cyst.  A  narrow  band-like  shadow  between  the  mass 
and  the  diaphragm  seemed  to  indicate  its  origin  by  rupture  from  the 
liver.     In  the  left  lung  an  oval,  homogeneous  shadow  was  regarded 

as  a  second  and  intact  cyst. 

Fig.  (»•") 


Bilateral  pulmonary  echinococcus  cyst.      (Behrenroth.) 

Serum  Diagnosis. — Two  methods  have  been  used.  Fleig  and  Lis- 
bonne1  were  the  first  to  investigate  the  precipitin  method.  Twelve 
drops  of  the  patient's  serum  were  added  to  2  c.c.  of  hydatid  fluid. 
Precipitation  of  the  fluid  occurred  after  some  hours,  the  material 
being  kept  meanwhile  at  40°  to  42°.  This  test  has  also  been  performed 
by  Welsh  and  Chapman,2  Weinberg3  and  Bettencourt.4  The  reaction, 
however,  is  not  constant. 

The  second  method,  by  complement-fixation  (Bordet-Gengou  reac- 
tion), was  first  used  by  Guedini.5  It  has  been  employed  by  Betten- 
court,6 Weinberg,7  Parvu  and  Laubry,8  Krueter,9  Jianu,10  Lippman,11 
and  others.  Lippman  collected  41  cases  of  echinococcus  disease  in 
man,  in  which  the  test  had  been  tried  and  two  of  his  own.    Of  the  43 

1  Itecherches  sur  un  sere-diagnostic  du  cyste  hydatique  par  la  methodc  des  precipitines, 
Comptes  rend.  soc.  de  biol.,  1907,  lxii,  1198. 

2  Lancet,  London,  May  9,  1908,  and  1909,  i,  1103. 

3  Comptes  rend,  de  la  soc.  de  biol.,  January  29,  1909,  No.  3,  vol.  Ixvi. 

4  Arch,  de  Real  Institute  Bacteriologico  Camara  Pestana,  Bd.  ii,  H.  3,  S.  361,  quoted 
from    Jianu.  Wiener,    klin.    Woch.,    1909,    No.    42. 

5  Quoted  from  Centralbl.  f.  Bakt.,  xl,  464:   ref.  and  also  ibid.,  1908,  xli,  716. 

6  Loc.  cit.  '  Loc.  cit. 

8  Comptes  rend,  de  la  soc.  de  biol.,  1909,  T.  Ixvi,  p.  467,  No.  11. 

9  Munch,  med.  Woch.,  1909,  No.  36;    also  Beitr.  z.  klin.  Chir.,  Bd.  lxxvi. 
1,1  Wiener  klin.  Woch.,  October  21,  1909,  No.  42. 

11  Berliner  klin.  Woch.,  January  3,  1910. 


ECHINOCOCCUS  DISEASE  OF   THE  LUNG  415 

cases,  only  2  were  negative,  both  of  whom  later  showed  the  reaction. 
The  method,  therefore,  appears  quite  trustworthy  and  offers  much 
promise.  Jianu  takes  no  more  than  3  e.e.  of  the  patient's  blood,  and 
allows  it  to  stand  for  five  to  six  hours  in  the  thermostat,  in  order  to 
obtain  the  maximum  of  complement.  The  antigen  is  obtained  from  the 
eehinococcus  fluid  of  sheep  or  cattle,  collected  fresh  and  under  aseptic 
precautions  in  the  slaughter  house.  An  extract  of  the  fluid  may  also 
be  used.  The  presence  or  absence  of  hemolysis  is  noted  on  the  addi- 
tion of  these  substances  to  a  2  per  cent,  emulsion  of  sheep's  red-blood 
corpuscles.  No  constant  relation  appears  to  obtain  between  eosino- 
philia  and  the  reaction  of  fixation.  The  reaction  may  last  long  after 
operation. 

Thoracentesis. — The  diagnosis  has  often  been  made  in  this  way. 
The  procedure  is  attended  by  considerable  danger,  however,  and 
cannot  be  recommended.  Puncture  of  the  cyst  is  likely  to  be  followed 
by  the  escape  of  eehinococcus  fluid  into  the  space  between  the  wall  of 
the  sac  and  the  connective-tissue  capsule,  thence  into  the  bronchi 
or  through  the  canal  of  puncture  to  the  pleural  cavity.  The  irritating 
fluid  excites  cough,  during  which  the  sac  and  the  escaped  fluid  are 
subjected  to  increased  tension.  Rupture  of  the  ■sac  is  likely  to  be  a 
consequence.  Symptoms  of  severe  intoxication,  as  urticaria,  gastro- 
intestinal disturbances,  faintness,  collapse,  delirium,  and  even  coma 
and  death  may  result.  Edema  of  the  lung  may  ensue.  Pulmonary 
suppuration,  empyema,  or  pyo-pneumothorax  may  follow  the  evacua- 
tion of  septic  fluid.  Obstruction  of  the  bronchi  by  fluid,  cysts,  or 
cyst  membrane  or  the  entrance  of  air  into  the  pleural  sac  may  cause 
suffocation.  Maydl1  has  reported  11  deaths  among  16  cases  in  which 
thoracentesis  was  performed.  Many  additional  fatalities  have  since 
been  reported.  O'Conor2  refers  to  an  unusual  case  in  which  the  expec- 
toration of  two  liters  of  fluid  occurred  while  the  attendant  was  cleaning 
a  syringe  in  preparation  for  exploratory  puncture.  If  the  disease  is 
suspected  an  exploratory  incision,  with  full  preparations  for  a  surgical 
operation,  should  be  performed.  If  the  case  is  under  suspicion  for 
pleural  effusion  and  eehinococcus  fluid  is  obtained  by  puncture,  opera- 
tion should  be  undertaken  at  once. 

Examination  of  uninfected  fluid  may  readily  suggest  the  diagnosis. 
A  clear,  watery  fluid,  of  a  low  specific  gravity,  with  considerable 
sodium  chloride  and  only  traces  of  albumin,  is  not  likely  to  be  confused 
with  any  other  condition.  In  some  instances,  however,  the  specific- 
gravity  is  high  and  the  amount  of  albumin  considerable.  Infection 
of  the  cyst  is  likely  to  mask  the  appearance  of  the  fluid,  which  may 
then  vary  from  a  merely  turbid  material,  with  a  sediment  of  poly- 
nuclear  cells,  to  frank  pus.  Positive  evidence  of  the  character  of  the 
process  will  be  furnished  by  the  discovery  of  scolices  or  hooklets  in 
the  sediment.    Long  search  may  be  necessary. 

1  Ueber  Echinokokkus  der  Pleura,  Wien,  1891. 

2  Lancet,  London,  1903,  i,  1433. 


416  DISEASES  OF   THE  LUNGS 

The  pulmonary,  pleural,  or  subdiaphragmatic  site  of  an  echinococcus 
cyst  may  he  difficult  or  impossible  of  determination.  The  various 
forms  may  coexist.  In  Patella's1  ease  the  diagnosis  before  operation 
was  pleural,  after  operation  hepatic,  and  at  autopsy  pulmonary 
echinococcus:  The  physical  signs  of  centrally  placed  pulmonary 
cysts  may  be  slight  or  absent.  Cysts  near  the  periphery  of  the  lung 
present  the  same  signs  as  in  pleural  echinococcus,  but  the  history 
may  be  helpful  in  the  differentiation.  In  the  pulmonary  disease  pain 
is  less  often  present,  while  cough  and  hemoptysis  are  more  prominent 
features.  1 ) yspnea  is  common  to  both  pleural  and  pulmonary  forms, 
but  is  more  often  paroxysmal  when  the  lung  is  affected.  Perforation 
into  the  bronchi  occurs  more  frequently  with  pulmonary  cysts.  Sub- 
diaphragmatic cysts  likely  to  be  confused  with  those  in  the  lung  usually 
develop  in  the  upper  part  of  the  liver  or  the  space  between  the  liver 
and  the  diaphragm.  The  clinical  picture  is  then  more  like  the  pleural 
than  the  pulmonary  form.  Pain  may  or  may  not  be  a  feature,  depend- 
ing on  the  presence  or  absence  of  infection  extending  through  the 
diaphragm  to  the  pleura.  Cough  and  hemoptysis  are  not  likely  to 
occur  unless  rupture  has  taken  place.  Paroxysmal  dyspnea  is  not  a 
prominent  feature  and  rupture  into  the  lung  is  less  frequently 
observed.  When  it  does  occur,  however,  the  sputum  is  likely  to  be 
ochre-yellow  in  color,  and  to  respond  to  the  tests  for  bile  pigments. 
Jaundice  may  be  present.  Downward  displacement  of  the  liver  is 
commonly  more  marked  in  the  subdiaphragmatic  site.  The  presence 
of  the  diaphragm  shadow  above  the  growth  may  be  an  important 
sign.  If  the  tumor  projects  below  the  margin  of  the  ribs,  hydatid 
fremitus  may  be  felt.  If  a  zone  of  resonance  can  be  determined  between 
the  growth  and  the  hepatic  dulness  it  is  strongly  in  favor  of  a  pulmonary 
process. 

Of  the  various  diseases  with  which  pulmonary  hydatids  are  likely 
to  be  confused,  tuberculosis  occupies  first  place.  In  a  majority  of  the 
cases  a  probable  diagnosis  of  this  disease  has  been  made  before  rup- 
ture occurs.  The  two  affections  have  much  in  common  and  mistakes 
are  at  times  inevitable.  A  history  of  tuberculosis  or  opportunity  for 
contagion,  persistent  cough  with  mucopurulent  or  purulent  sputum, 
loss  of  weight  and  strength,  night  sweats  and  evening  rise  of  tempera- 
ture are  suggestive  of  tuberculosis.  The  dyspnea  is  seldom  marked. 
Fibrinous  or  serofibrinous  pleurisy,  as  an  apparently  primary  affection 
without  symptoms  or  signs  referable  to  other  organs,  and  hemoptysis 
as  an  initial  symptom  or  early  in  the  course  of  an  apparently  mild 
pulmonary  disturbance,  are  suggestive  of  tuberculosis.  So  also  in 
the  general  examination  may  be  phlyctenular  conjunctivitis,  corneal 
scars  (if  trauma,  gonorrhea,  or  syphilis  can  be  excluded),  lupus, 
cicatrices  from  cervical  adenitis,  and  ischiorectal  abcesss.  Examina- 
tion of  the  lungs  may  be   negative   or  show  evidence  of  involve- 

1  Quoted  from  Maydl,  Ueber  Echinokokkus  der  Pleura,  Wien,  1891,  p.  71. 


ECHINOCOCCUS  DISEASE  OF  THE  LUNG  417 

ment  of  the  apices  as  indicated  by  retraction,  rales,  or  signs  of  pul- 
monary consolidation.  Bilateral  apical  lesions  are  not  uncommon. 
With  echinococcus  disease  of  the  lung,  on  the  other  hand,  the  cough 
is  likely  to  be  dry,  the  dyspnea  more  marked,  the  general  health  little 
if  any  disturbed,  and  the  course  to  be  afebrile.  Pleurisy  or  hemoptysis 
are  usually,  but  not  always,  preceded  by  pulmonary  symptoms  or 
signs.  Although  cysts  may  be  apical,  they  are  more  commonly  basal, 
unilateral,  and  right  sided.  The  affected  region  is  prominent  rather 
than  retracted  and  the  signs  are  those  of  pleural  effusion.  Mainten- 
ance of  good  nutrition  and  signs  of  extensive  intrathoracic  disease 
may  be  striking. 

Pulmonary  echinococcus  may  also  be  confused  with  pleural  effusion. 
A  history  of  persistent  cough,  dyspnea  of  a  paroxysmal  character, 
and  repeated  hemoptysis  is  more  frequently  to  be  obtained  in  the 
former.  Pain  is  more  likely  to  be  a  prominent  feature  with  pleurisy. 
In  both  the  base  of  the  lung  is  likely  to  be  affected.  The  signs  of 
intact  cysts  are  those  of  encysted  pleural  effusion.  As  sacculated 
exudates  are  usually  purulent,  with  an  acute  onset,  toxic  symptoms, 
chills,  fever  and  leukocytosis,  an  insidious  onset  and  latent  course  may 
suggest  echinococcus  disease.  A  location  elsewhere  than  at  the  base 
may  be  more  definitely  suggestive.  Free  pleural  fluid  presents  a 
slightly  curved  upper  margin  (Damoiseau's  curve),  while  the  contour 
of  cysts  is  rounded  with  the  convexity  upward.  Shifting  dulness  may 
be  demonstrated  with  an  effusion,  but  is  absent  with  cysts.  A  zone 
of  resonance  between  the  dull  area  and  the  base  of  the  lung,  persist- 
ence of  the  diaphragm  shadow  on  the  affected  side,  abrupt  transition 
from  dulness  to  resonance,  and  from  diminished  or  absent  to  normal 
or  exaggerated  breathing,  absence  of  bronchophony  or  asgophony 
speak  for  cyst  rather  than  pleural  fluid. 

Tumors  of  the  lung,  the  pleura,  or  the  mediastinum  may  be  con- 
sidered. Malignant  growths  are  for  the  most  part  in  question.  The 
local  signs  are  much  the  same,  but  the  margin  of  a  malignant  growth 
is  likely  to  present  a  different  outline.  More  intense  pain,  stridor, 
paralysis  of  the  vocal  cords,  dysphagia,  dilatation  of  the  cervical  or 
thoracic  veins,  superficial  metastases,  resistance  and  induration  of 
the  thoracic  wall,  a  more  rapid  course,  and  progressive  cachexia  are 
likely  to  be  observed  with  such  tumors.  An  accumulation  of  bloody 
pleural  fluid  is  much  less  common  with  echinococcus  disease.  Intra- 
thoracic aneurysm  may  simulate  an  echinococcus  cyst,  but  the  differ- 
entiation is  usually  easy. 

A  ruptured  and  infected  echinococcus  cyst  may  give  rise  to  pul- 
monary abscess  or  gangrene  which  may  then  resemble  similar  pro- 
cesses from  other  causes.  Certain  features  of  the  history,  already 
mentioned,  may  suggest  echinococcus  disease.  If  the  condition  is 
known  to  have  followed  lobar  pneumonia  the  inhalation  of  foreign 
bodies,  submersion,  etherization,  operations  about  the  upper  respira- 
tory tract,  or  on  an  individual  known  to  be  the  subject  of  bronchial 
27 


4  IS  DISEASES  OF   THE  LUNGS 

or  pulmonary  inflammation,  or  trauma,  or  if  it  occurs  in  the  course  of 
suppuration  anywhere  in  the  body,  especially  in  the  pleura  or  abdo- 
men, a  different  etiology  may  be  established.  The  sputum  may  show 
elastic  tissue  or  shreds  of  the  lung,  and  the  signs  of  cavity  may  be 
present  on  physical  examination.  Actinomycosis  and  tuberculosis 
should  be  excluded  by  repeated  examinations  of  the  sputum.  The 
finding  of  booklets,  scolices,  or  cyst  membrane  may  be  the  first  indi- 
cation that  echinococcus  disease  is  the  cause. 

Prognosis. — The  outlook  with  pulmonary  echinococcus  allowed  to 
run  its  course  untreated  is  better  than  with  the  pleural  form,  but  is 
yet  very  unfavorable.  Recovery  from  death  of  the  parasite  has  not 
been  reported  for  pulmonary  hydatids.  The  expectation  of  life  without 
treatment  cannot  be  definitely  stated.  Left  to  itself  the  cyst  gradually 
increases  in  size  until  rupture  takes  place.  Of  Hearn's1  144  cases  of 
pulmonary  and  pleural  echinococcus  collected  from  the  literature, 
82  (56.9  per  cent.)  died  and  62  (43  per  cent.)  recovered.  Recovery 
was  due  to  the  expectoration  of  the  hydatids  in  45,  to  simple  punc- 
ture in  5,  puncture  or  incision  and  evacuation  by  the  bronchi  in  7, 
incision  of  the  thoracic  wall  in  2,  and  puncture  with  the  injection  of 
iodin  or  evacuation  by  the  intestine  in  one  each.2  Death  when  it 
occurs  is  usually  due  to  suffocation,  hemorrhage,  pneumothorax,  or 
sepsis.  It  may  be  sudden  or  life  may  be  prolonged,  the  patient  grad- 
ually dying  of  asthenia.  It  is  relatively  uncommon  even  in  the 
recovered  cases,  for  complete  relief  from  pulmonary  symptoms  to 
follow  spontaneous  evacuation  by  the  bronchi.  Infection  of  the  cyst 
cavity  and  the  neighboring  or  remote  parts  of  the  lung  is  likely  to 
leave  a  permanently  damaged  pulmonary  tissue.  Reimplantation 
of  the  growth  is  a  possible  sequel  to  evacuation  into  the  bronchi,  as 
already  mentioned.  The  chance  of  recovery  is  far  better  from  sur- 
gical intervention. 

Treatment. — There  is  no  medical  treatment.  Simple  puncture 
with  or  without  the  injection  of  iodin,  carbolic  acid,  corrosive  subli- 
mate, or  other  substances  has  been  frequently  and  at  times  success- 
full}'  performed.  It  is,  however,  a  dangerous  method  and  should  be 
strongly  condemned.  The  objections  to  puncture  have  already  been 
sufficiently  emphasized  (see  p.  415).  If,  as  occasionally  happens, 
exploratory  puncture,  undertaken  for  a  suspected  pleural  effusion, 
discloses  echinococcus  fluid,  the  danger  of  its  escape  into  the  bronchi 
should  be  avoided  by  an  immediate  resort  to  surgical  intervention 

Intact  Cysts. — The  condition  of  the  pleura  has  an  important  bearing 
on  the  operative  procedure.  If  the  pleural  sac  is  already  obliterated, 
the  operation  is  relatively  simple  and  the  danger  of  artificial  pneumo- 
thorax is  eliminated.  As  it  is  never  possible  with  certainty  to  know 
in  advance  whether  the  pleura  is  partially  or  wholly  free  or  adherent 
it  is  safer  to  proceed  in  all  cases  as  cautiously  as  if  it  were  free.    The 

1  Kystes  hydatiquea  du  pounion  ct  de  la  plevrc,  Paris,  1<S75. 

2  The  total  here  as  in  Hearn's  table  amounts  to  only  61. 


ECHINOCOCCUS  DISEASE  OF   THE  LUNG  419 

incision  is  made  over  the  site  of  the  tumor.  Subperiosteal  costatectomy 
is  done  over  a  sufficient  area,  and  if  the  pleura  is  found  to  be  obliter- 
ated, the  lung  may  be  incised  with  care  not  to  open  the  cyst  mem- 
brane. Having  opened  the  connective-tissue  capsule  an  attempt  may 
be  made  to  remove  the  cyst  entire.  If  this  cannot  be  accomplished 
without  rupture  the  cyst  membrane  may  be  drawn  into  the  wound 
of  operation  and  aspirated  in  such  a  manner  that  its  contents  will  not 
escape  into  the  connective-tissue  capsule.  The  collapsed  cyst  may 
then  be  shelled  out  from  its  capsule  and  the  cavity  then  be  lightly 
packed  with  gauze.  Irrigation  with  antiseptic  fluids  is  not  to  be 
advised.  In  cases  uncomplicated  by  pulmonary  inflammation  or  indura- 
tion the  defect  in  the  lung  is  rapidly  closed.  In  cases  in  which  the 
pleural  sac  is  free,  and  without  urgent  symptoms,  the  operation  may 
be  done  in  two  stages,  at  the  first  of  which  the  two  layers  of  the  pleura 
are  united  by  suture  about  the  margin  of  the  field  of  operation.  An 
interval  is  then  allowed  to  elapse  before  pneumotomy  is  done.  An 
anchor  stitch  through  the  pulmonary  pleura  and  including  also  some 
of  the  pulmonary  tissue  may  prove  a  safeguard  against  pulmonary 
retraction  and  sudden  pneumothorax  during  the  manipulations. 

Careful  localization  of  the  cyst  should  precede  operation.  For 
this  purpose,  examination  with  the  x-rays  is  almost  indispensable.  If 
the  location  of  the  cyst  is  doubtful  or  if  it  appears  to  occupy  a  central 
position,  Garre1  suggests  fixation  of  the  lung  at  one  or  two  places  by 
a  strong,  deep  suture,  free  opening  of  the  pleura  and  exploration  of 
the  affected  lobe  by  the  index  finger,  or  if  necessary  by  the  whole  hand 
introduced  into  the  pleural  space. 

Ruptured  Cysts. — After  evacuation  has  been  partly  or  wholly  effected 
by  way  of  the  bronchi  the  indications  for  operation  are  less  clear, 
and  opinion  is  divided  between  an  expectant  policy  and  operation. 
During  the  period  immediately  following  rupture  the  patient  is  in 
danger  of  suffocation  from  the  flooding  of  the  air  passages  with  fluid, 
cysts,  or  cyst  membrane.  In  some  instances- cysts  and  cyst  membrane 
are  expectorated  at  intervals  over  a  considerable  period,  and  the 
danger  period  is  correspondingly  prolonged.  Suppuration  of  the  cyst 
commonly  precedes  or  soon  follows  rupture,  and  if  not  immediately 
fatal,  greatly  endangers  the  ultimate  restoration  of  the  pulmonary 
tissue  to  normal.  Fatal  hemorrhage  may  also  occur.  There  is  also 
the  possibility  of  dissemination  of  the  parasite  into  other  parts  of  the 
lung.  The  danger  of  this,  however,  is  as  yet  little  known.  One  must 
weigh  on  the  one  hand  the  dangers  incident  to  rupture  and  on  the 
other  those  of  the  operation  itself.  In  general  it  may  be  said  that 
with  the  progress  already  made  in  thoracic  surgery  the  patient's 
chances  are  better  in  the  hands  of  an  experienced  operator,  when  the 
cyst  is  incompletely  evacuated  or  with  evidence  of  persistent  suppura- 
tion.   Following  rupture  into  the  pleura  operation  is  also  indicated. 

1  Garre  and  Quincke,  Grundriss  der  Lungenchirurgie,  Fischer,  Jena,  1903,  p.  SI. 


420  DISEASES  OF  THE  LUNGS 

PULMONARY   DISTOMATOSIS    (LUNG-FLUKE   DISEASE.) 

Parasitic  Hemoptysis. — Etiology. — This  interesting  disease  is  en- 
demic in  Japan  and  China.  It  has  been  reported  also  from  Korea  and 
the  Philippine  Islands.  It  is  said  that  in  certain  parts  of  Formosa 
15  per  cent,  of  the  population  are  affected.  Inouye1  found  that  in 
Tama  (in  the  Distoma  region)  among  38  patients,  there  were  28 
(73.6  per  cent.)  with  the  disease  in  other  members  of  their  families, 
and  states  that  it  is  not  uncommon  for  whole  families  to  be  swept  out 
of  existence  by  it.  Paul2  reports  that  39  per  cent,  of  the  school  boys 
in  Kumamoto  were  affected.  The  prevalence  varies  considerably  in 
different  localities.  Among  20,793  patients  in  the  hospital  at  Okayama 
(1891-1897)  87  (0.4  per  cent.)  had  the  disease.  In  Matuyama  2.1G 
per  cent.,  in  Kumamoto  5.9  per  cent.,  and  in  Tokushima  14.3  per  cent, 
of  patients  with  respiratory  disease  were  sufferers  from  it.3  Imported 
cases  are  in  rare  instances  found  in  various  countries.  Stiles4  and 
Fehleisen  and  Cooper5  have  reported  instances  of  human  infection 
in  America,  imported  from  Japan.  Null6  observed  a  case  in  a  Korean. 
Abend's7  case  may  have  originated  in  America.  The  disease  occurs 
also  in  dogs,  cats,  swine,  cattle,  and  tigers.  In  Okayama  7  of  130 
dogs  killed  in  1897  were  infected. 

Mountainous  regions  appear  to  be  most  affected.  A  large  proportion 
of  the  cases  occur  in  males.  Of  481  patients  reported  by  Inouye, 
426  (88.5  per  cent.)  were  men  and  55  (11.4  per  cent.)  women.  The 
disease  is  more  common  among  peasants,  and  from  sixteen  to  thirty 
years  of  age. 

The  Parasite. — This  was  first  described  in  1878  by  Kerbert,8  under 
the  name  of  Distoma  Westermanni,9  the  specimen  being  obtained 
from  the  lungs  of  a  tiger.  Its  relation  with  parasitic  hemoptysis  was 
established  in  the  course  of  several  years  by  the  combined  efforts  of 
several  workers.  The  eggs  of  the  parasite  were  discovered  in  the 
sputum  of  a  Japanese  in  1878  by  Baelz,10  but  were  at  first  wrongly 
regarded  as  protozoa.  Manson11  also  discovered  the  eggs  in  Amoy 
and  obtained  a  specimen  of  the  worm  found  by  Ringer  (1879)  in  the 
bronchi  of  a  man  from  Formosa.  This  specimen  was  named  Distoma 
Ringeri  by  Cobbold.12  Its  identity  with  the  worm  found  in  the  lungs 
of  a  tiger  by  Kerbert13  was  discovered  by  Leuckart. 

I  Zeit.  f.  klih.  Med.,  1903,  vol.  1.  2  Lancet,  December  19,  1896. 

3  Inouye,  loc.  cit. 

4  Johns  Hopkins  Hosp.  Bull.,  July  and  August,  1904. 
6  Jour.  Amer.  Med.  Assoc,  February  26,  1910. 

e  Northwest  Med.,  December,  1911.  7  Deut.  Arch.  f.  klin.  Med.,  1910,  c,  501. 

8  Zool.  Anzeiger,  No.  12,  p.  271. 

9  Synonyms. — Gregarina  pulmonalis  s.  fusca.,  Baelz,  1880;  Distoma  Ringeri,  Cobbold, 
1880;  Distoma  pulmonalis  Kinono,  Suga  and  Yamagata,  1881;  Distoma  pulmonale, 
Baelz,  18S3;    Mesagonimus  Westermanni  Rail,  1890. 

10  Ueber  parasitare  Hamoptoe.  Gregarinosis  pulmonum,  Centralbl.  f.  d.  ges.  med. 
Wissenschaften,  1880,  No.  39. 

II  China  Imperial  Maritime  Customs,  Med.  Rep.,  1880,  vol.  xx. 

12  Jour.  Quekett  Micr.  Club.,  vol.  vi,  pp.  139-140.  I3  Loc.  cit. 


P  ULMONA  R  Y  DIS  TOM  A  TOSIS 


421 


The  worm  is  a  plump,  oval,  or  pyriform  spinose  fluke,  7.5  to  16  mm. 
long,  4  to  8  mm.  broad,  and  2  to  5  mm.  thiek.  Fresh  specimens  are 
of  a  pinkish  or  reddish-brown  eolor.  The  testicles  and  ovary  are 
branched,  the  intestinal  ceca  unbranched.1    The  eggs  are  oval,  golden 


Fig.  66 


Pulmonary  distoma.     Adult  woim.      X  2. 
Fig.  67 


Eggs  expressed  from  worm.      X  200. 
Fig.  68 


Egg  and  empty  shell.      X  200. 


yellow,  thin  shelled,  80  to  100  by  50  to  60^,  with  an  operculum  at 
one  end,  and  contain  finely  granular  masses.  They  are  larger  than 
the  eggs  of  other  parasites  commonly  found  in  man,  and  can  even  be 


1  For  more  detailed  descriptions,  see  Stiles  and  Hassall,  1900,  pp.  560-611. 


422 


DISEASES  OF  THE  LUNGS 


seen  with  the  naked  eye  as  brownish  speeks,  when  material  containing 
them  is  pressed  into  a  thin  layer  between  cover-glass  and  slide  and 
examined  by  transmitted  light.  They  most  resemble  the  eggs  of 
Bothriocephalus  latns,  from  which  they  can  be  differentiated  by  their 
larger  size.  The  eggs  contain  no  embryo  when  discharged.  As  many 
as  12,000  eggs  may  be  expectorated  in  a  day. 

Fig.  69 


Eggs  of  bothriocephalus  latus  in  stool.     X  200. 

The  source  of  infection  of  man  is  unknown.  Nakahama1  succeeded 
in  developing  embryos  from  eggs  kept  in  water  at  30°  to  35°  C,  and 
changed  every  day  or  every  other  day  for  four  weeks.  It  is  probable 
that  the  embryos  enter  a  snail  or  fish  as  intermediate  hosts  and  that 
human  infection  follows  the  ingestion  of  infected  food.  Of  this  there 
is  no  direct  evidence,  but  it  is  suggested  by  analogy  with  other  flukes 
(Fasciola  hepatica  and  Opisthorchis  felineus)  the  life  history  of  which 
is  better  known.  Contaminated  water  is  also  a  possible  source.  The 
portal  of  entry  and  the  course  taken  to  the  lungs  is  uncertain,  but 
it  is  assumed  by  many  Japanese  investigators  that  the  worm  enters 
the  intestinal  canal  with  food  or  drink,  perforates  the  intestinal  wall, 
and  finally  makes  its  way  into  the  lung. 

Pathology. — The  worm  is  found  in  cystic  cavities  about  the  size 
of  a  hazel-nut,  deep  within  the  lung  or  more  commonly  superficially 
placed  just  beneath  the  pleura.  Within  the  lung  they  may  be  felt 
as  small  nodules.  At  the  surface  they  may  project  as  hemispherical 
prominences  of  a  bluish-gray  color.  As  many  as  twenty-eight  may 
be  found.     The  walls  of  the  cysts  are  formed  of  connective  tissue, 


1  Quoted  from  Inouye,  loc.  cit.,  p.  132. 


PULMONARY  DISTOMATOSIS  423 

the  inner  surface  of  which  is  usually  smooth.  In  each  cavity  from  one 
to  three  worms  are  present.  A  reddish,  dirty  brown,  or  chocolate- 
colored  slimy  fluid,  containing  blood  cells,  debris,  large  numbers  of 
eggs,  and  Charcot-Leyden  crystals  may  also  be  found.  Empty  cavities 
may  be  present.  Neighboring  cysts  at  times  communicate  with  each 
other  by  sinuous  channels,  and  rupture  of  the  intervening  walls  may 
result  in  irregular  cavities  of  considerable  size.  The  cavities  commu- 
nicate with  the  bronchi  by  one  or  more  openings.  Yamagiwa1  regarded 
the  pulmonary  tissue  as  the  site  of  the  cavity.  Inouye2  found  in  cats 
that  the  inner  surface  of  the  cavity  was  covered  with  pavement 
epithelium  and  in  the  outer  wall  were  non-striated  muscle  fibers, 
and  believes  the  bronchi  the  site  of  formation.  Tanaka3  found  the 
cavities  to  be  due  to  dilatation  of  the  smaller  bronchi  in  a  dog.  The 
lung  tissue  appeared  to  be  the  site  of  the  cavities  in  a  man  on  whom 
a  postmortem  examination  was  made.  The  demonstration  of  the 
parasite  in  other  parts  of  the  body  than  the  lungs  makes  it  probable 
that  pulmonary  infection  is  not  confined  to  the  bronchi.  Pleural 
adhesions  are  common. 

Otani,4  Yamagiwa,5  and  Inouye  and  Katsurada6  have  reported 
autopsies  on  cases  with  cerebral  infection.  Cysts  and  eggs  were  found 
in  the  right  frontal,  and  cysts,  two  worms,  and  eggs  in  the  occipital 
lobes  (Otani).  Cysts  and  eggs  were  present  in  the  temporal  lobe 
and  in  the  optic  thalamus  (Inouye).  Disseminated  dark  gray,  resis- 
tant areas  containing  eggs  were  found  in  the  cortex  of  the  occipital, 
parietal,  and  central  lobes.  These  foci  showed  round-celled  infiltra- 
tion at  their  periphery  (Yamagiwa).  The  lungs  were  infected  in  two 
of  the  cases  (Otani  and  Yamagiwa).  Infection  of  the  liver,  intestinal 
wall,  peritoneum,  diaphragm,  cervical  glands,  upper  part  of  Poupart's 
ligament,  orbital  cavity,  scrotum,  and  lower  eyelid  has  also  been 
observed  (Inouye) .  Miura7  found  numerous  areas  resembling  miliary 
tubercles  and  containing  eggs  in  the  great  omentum,  and  Tanaka8 
found  several  similar  nodules  in  the  peritoneum.  In  neither  case 
could  the  mother  worm  be  found. 

Symptoms. — Pulmonary  infection  is  the  usual  type  of  the  disease. 
The  onset  is  commonly  insidious.  The  patient  first  notices  a  gradually 
increasing  cough  and  expectoration,  which  are  likely  to  be  more  severe 
in  the  morning  on  rising.  The  cough  is  seldom  severe  enough  to  dis- 
turb sleep.  In  rare  instances  it  is  paroxysmal,  and  asthmatic  attacks 
may  be  simulated.  Thoracic  pain  is  not  uncommon.  It  was  noted 
among  92  patients  in  34  (36.9  per  cent.)  of  whom  28  had  thoracic 
retraction  (Inouye),  and  is  doubtless  caused  by  pleuritis.    Dyspnea, 

1  Virchow's  Arch.,  1892,  exxvii,  452.  2  Loc.  cit. 

3  Wiener  klin.  Woch.,  1911,  No.  2,  p.  49. 

4  Zeit.  d.  med.  Gesellsch.  in  Tokio,  1887,  Bd.  i.  See  Yamagiwa,  Virchow's  Arch., 
1890,  cxix,  447. 

6  Ibid.  6  Inouye,  loc.  cit. 

7  Virchow's  Arch.,  1889,  Bd.  cxvi.  s  Loc.  cit. 


424  DISEASES  OF  THE  LUNGS 

palpitation,  and  cardiac  apical  murmurs,  due  to  anemia  following 
hemoptysis,  arc  sometimes  observed.  Hoarseness  is  occasionally 
present. 

The  sputum  varies  in  color  from  yellow  to  rusty  brown  or  dark  red, 
from  admixture  of  eggs  and  blood.  It  also  contains  mucus  and  pus, 
and  may  have  a  peculiar  odor  from  the  presence  of  blood.  It  may  be 
absent  for  a  time,  is  usually  small  in  amount,  but  may  reach  100  c.c. 
a  day.  The  only  distinctive  feature  of  the  sputum  is  the  presence  of 
the  eggs,  which  can  be  identified  with  certainty  only  on  microscopic 
examination.  Blood,  pus,  mucous  threads,  alveolar  and  bronchial 
cells  may  also  be  found.  Charcot-Leyden  crystals  are  almost  invari- 
ably present.  Structures  resembling  Curschmann's  spirals  were 
found  in  17  (18.4  per  cent.)  of  92  cases  examined  by  Inouye. 
They  are  3  to  4  cm.  long  and  about  1  mm.  thick,  of  a  pale  red  or  brown 
color.  Taylor  and  Mimachi  each  found  an  expelled  worm  in  the  spu- 
tum.   Mimachi's  case  was  complicated  with  pulmonary  tuberculosis. 

Hemoptysis  is  the  most  striking  feature  of  the  disease.  It  is  common 
but  not  invariably  present,  and  occurs  as  bloody  points,  streaks,  or 
frank  hemoptysis.  Baelz  has  reported  a  case  in  which  there  was  the 
loss  of  a  pound  of  blood  within  a  few  hours.  Bloody  sputum  is  more 
often  seen  during  the  colder  months  of  the  year,  after  excessive  physical 
or  mental  exertion,  the  use  of  alcohol  and  tobacco.  The  bleeding  has 
been  ascribed  to  disintegration  of  the  cyst  wall  and  erosion  of  blood- 
vessels. Inouye  suggests  that  the  parasite  sucks  blood  from  the 
cyst  wall,  which  continues  to  bleed  after  the  suction  is  stopped.  A 
severe  grade  of  anemia,  ending  fatally,  may  follow  repeated  attacks 
of  hemoptysis. 

On  physical  examination  the  patient  is  usually  found  to  be  well 
nourished.  Signs  of  pulmonary  disease  are  usually  lacking,  except  in 
severe  cases.  There  may  be  diminished  expansion  of  one  side.  Inouye 
finds  retraction  of  the  chest,  especially  in  the  infrascapular  region, 
among  the  most  common  signs.  This  is  due  to  pleuritis.  Slight  dul- 
ness,  an  increased  sense  of  resistance,  diminished  vesicular  or  broncho- 
vesicular  breathing,  and  dry  or  moist  rales  may  be  found.  The  signs 
of  cavity  formation  are  seldom  present.  A  patchy  distribution  of 
the  pulmonary  signs  is  suggestive  of  the  disease.  The  temperature 
is  usually  unelevated.    Night  sweats  are  uncommon. 

Complications. — Infection  of  the  brain  by  the  worms  or  their  eggs 
appears  to  be  one  of  the  most  common  and  serious  complications. 
Among  Inouye's  92  cases,  3  showed  cerebral  symptoms  (headache, 
vertigo,  weak  memory),  2  epilepsy,  and  1  epilepsy  and  left  hemiplegia. 
Inouye  has  collected  19  cases  with  cerebral  symptoms.  Among  them, 
8  had  general  and  6  unilateral  (2  right-  and  4  left-sided)  spasms. 
Five  had  hemiplegia.  Paresis  of  the  right  arm,  color  ring,  vertigo, 
psychic  blindness,  etc.,  were  also  observed.  It  seems  probable  that 
the  eggs  reach  the  brain  as  emboli,  gaining  entrance  to  the  circulation 
through  a  pulmonary  vein.    The  presence  of  worms  in  the  brain,  as 


PULMONARY  DISTOM ATOMS  425 

in  Otani's  case,  is  unexplained.  In  rare  instances  the  worm  has  been 
found  in  the  eyelid,  where  the  resulting  tumor  may  obstruct  vision 
Cases  of  hepatic  cirrhosis  with  ascites  have  been  described  in  which 
eggs  of  the  pulmonary  distoma  were  found  in  the  interstitial  tissue 
of  the  liver,  but  the  eggs  may  have  been  coexistent  with  cirrhosis 
from  another  cause. 

Diagnosis. — This  is  usually  easily  made  from  the  presence  of  the 
eggs  in  the  sputum.  A  mass  of  the  fresh  material  should  be  pressed 
in  a  thin  layer  between  slide  and  cover-glass  and  examined  with  the 
low  power  of  the  microscope.  The  presence  of  Charcot-Leyden  crys- 
tals alone  is  strongly  suggestive  of  the  disease  in  patients  who  live 
in  infected  regions  and  careful  and  repeated  search  for  the  eggs  should 
be  made.  In  cases  in  which  no  sputum  can  be  obtained,  as  in  young 
children  or  the  aged,  search  for  the  eggs  in  the  stools  may  be  successful. 
The  eggs  of  Bothriocephalus  latus  should  then  be  carefully  differen- 
tiated from  those  of  the  lung-fluke. 

Pulmonary  distomatosis  may  closely  simulate  tuberculosis  and  the 
two  diseases  may  be  combined.  In  the  former,  pulmonary  changes 
are  less  often  found  at  the  apices,  the  sputum  is  more  likely  to  be 
brown  in  color,  frank  hemoptysis  is  less  frequent,  the  disease  is  more 
often  afebrile,  and  the  nutrition  is  less  disturbed.  The  presence  of 
eggs  or  tubercle  bacilli  in  the  sputum  may  establish  the  diagnosis  of 
one  but  does  not  exclude  the  other. 

Prognosis. — This  is  usually  good  for  the  uncomplicated  pulmonary 
form,  which  may  last  from  a  few  to  twenty  or  thirty  years.  The 
viability  of  the  worms  is  unknown  but  it  is  probable  that  such  pro- 
tracted cases  are  due  to  repeated  infections.  It  is  said  that  the  disease 
gradually  subsides,  if  the  patient  leaves  an  infected  region.  The 
prognosis  of  the  cerebral  form  is  serious. 

Prophylaxis. — Reliable  preventive  measures  cannot  be  formulated 
until  the  life-history  of  the  parasite  is  established.  Until  then  the 
following  precautions  may  be  observed:  An  infected  region  may  be 
avoided.  The  sputum  of  infected  individuals  should  be  expectorated 
into  a  special  receptacle,  which  should  then  be  burned.'  Infected 
animals  (dogs,  cats,  swine)  should  be  killed.  Bathing  should  not  be 
practiced  in  infected  streams,  drinking  water  should  be  filtered  or 
boiled,  green  vegetables  should  be  thoroughly  washed,  and  snails 
and  fish  should  be  thoroughly  cooked,  when  used  for  food. 

Treatment. — There  is  no  specific  treatment.  When  possible,  patients 
should  leave  an  infected  region.  If  the  site  of  the  disease  can  be  located, 
surgical  interference  may  be  considered.  The  usual  superficial  site 
of  the  pulmonary  infection  is  of  favorable  moment  but  great  care 
should  be  taken  not  to  infect  an  intact  pleura.  The  operative  technique 
may  well  be  that  for  pulmonary  abscess  or  gangrene.  Pleural  pain 
and  hemoptysis  should  be  treated  by  rest  and  such  other  measures 
as  are  elsewhere  described  for  these  symptoms. 


126  DISEASES  OF  THE  LUNGS 

Hepatic  Distoma. — An  instance  of  pulmonary  invasion  by  a  species 

of  liwr  fluke  is  reported  by  De  Gouvea.1 

OTHER   PARASITES. 

Strongyloides. — Gage2  found  a  few  filariform  larvae  in  the  sputum 
and  enormous  numbers  of  rhabditiform  larvae  of  Strongyloides  intes- 
tinalis  in  the  stools  of  a  patient  who  later  came  to  postmortem  exami- 
nation. The  lungs  showed  numerous  areas  of  bronchopneumonia. 
The  intestinal  mucosa  was  everywhere  deeply  injected  and  showed 
extensive,  superficial  ulceration.  The  mucus  from  the  duodenum 
contained  large  numbers  of  adult  worms,  active  rhabditiform  larvae, 
and  numerous  eggs.  Adult  worms,  larvae,  and  eggs  were  found  in  the 
intestinal  wall.  Larvae  were  present  in  lymph  spaces  and  lymph 
vessels  of  the  intestine,  and  two  larvae  were  found  in  the  lung  by  means 
of  serial  sections.  Gage  suggests  that  invasion  of  the  lung  may  occur 
by  entrance  into  the  lymph  channels  of  the  intestine,  thence  into  the 
thoracic  duct,  the  subclavian  vein  and  the  blood  stream,  and  that 
swallowed  larvae  may  develop  into  adult  worms. 

Strongylus  Longevaginatus.3 — This  is  reported  once  in  the  lungs 
of  a  girl,  aged  six  years. 

Uncinaria. — Richard4  found  larvae  of  the  hook-worm  in  the  sputum 
from  a  patient  with  bronchitis. 

Ascaris. — Lucksch5  reports  the  case  of  a  man  shot  in  the  upper 
abdominal  region.  Death  followed  fifteen  days  later.  At  autopsy 
one  ascaris  was  found  on  the  left  side  and  another  on  the  right  in 
branches  of  the  pulmonary  artery.  It  seemed  probable  that  the 
worms  had  emerged  from  a  hole  in  the  common  bile  duct  and  entered 
an  opening  in  the  inferior  vena  cava,  thus  gaining  entrance  to  the 
venous  circulation. 

Cysticercus  Cellulosae. — Infection  of  the  lungs  with  larvae  of  the 
tenia  solium  is  rare.  Iviihn6  collected  seven  cases  and  added  one  of  his 
own.  From  three  to  sixteen  of  the  parasites  have  been  demonstrated 
in  the  lungs.  Other  organs  also  are  usually  infected.  The  lungs  may 
be  free  and  yet  large  numbers  may  be  present  in  other  parts  of  the 
body.  Infection  may  take  place  by  the  entrance  of  a  segment  or  ova 
of  the  tape-worm  into  the  stomach  through  the  pylorus  or  cardia. 

Cercomonas. — Litten7  found  cercomonas  (monas  lens)  in  the  sputum 
and  the  pleural  exudate  from  a  patient  with  pleurisy  with  effusion 
and  pneumothorax.  Tubercle  bacilli  were  also  present  in  the  sputum. 
Litten  refers  to  an  observation  by  Kannenberg  in  which  cercomonas 
was  found  in  lung  gangrene. 

1  Hilario  de  Gouvea,  La  Distomatose  pulmonaire  par  la  Douve  du  Foie,  Paris,  1895. 

2  Jour.  Med.  Research,  1910,  xviii,  177. 

3  Diesing,  Systema  Helminthum,  1851,  ii,  317. 

4  Postgrad.,  New  York,  1909,  xxiv,  475. 

6  Askariden  als  Emboli  in  der  Lungenarterie,  Wiener  klin.  Woch.,  1905,  No.  15,  p.  377. 

6  Cysticerkus  cellulosae  in  den  Lungen,  Inaug.  Diss.,  Leipzig,  1905. 

7  Berl.  klin.  Woch.,  May  3,  1886. 


CHAPTER  XXVI. 
TUMORS  OF  THE  BRONCHI  AND  LUNG. 

BENIGN    TUMORS    OF   THE   LUNG. 

These  are  of  little  clinical  interest,  and  occur  only  in  very  rare 
instances,  being  usually  first  discovered  at  the  postmortem  examina- 
tion. Fibromata  have  been  described  as  small,  discrete  masses,  vary- 
ing in  size  from  a  millet  seed  to  a  hazel  nut.  They  are  usually 
peribronchial  and  are  probably  the  result  of  inflammatory  processes. 
Ferkel1  reports  a  case  of  fibromyoma  in  the  apex  of  the  left  lung 
the  size  of  a  lemon.  Osteomata  are  also  occasionally  seen  as 
rounded  nodules,  seldom  exceeding  the  size  of  a  pea  or  more  com- 
monly as  masses  of  irregular  shape  with  jagged  projections.  An 
unusual  instance  is  reported  by  Port  and  referred  to  by  Virchow.2 
In  this  case,  a  more  or  less  circumscribed  tumor-like  mass  the 
size  of  the  fist  occupied  the  right  upper  lobe.  A  large  elongated 
bony  projection  extended  from  it  toward  the  root  of  the  lung,  and 
several  isolated  smaller  nodules  were  found  in  the  upper  and  lower 
lobes.  In  Cohen's3  case,  there  was  a  diffuse  formation  of  bone  in  the 
greater  part  of  the  right  upper  lobe.  A  distinction  should  be  made 
between  calcareous  deposits  in  pathologic  tissue  and  true  osteoma. 
Lipomata  are  very  uncommon,  but  may  be  seen  as  globular  masses 
of  fatty  tissue  in  the  interlobar  or  subpleural  region.  Primary  cartila- 
ginous tumors,  with  or  without  an  apparent  relation  with  the  bronchi, 
have  been  reported  by  Wagner,4  Virchow,5  Lesser,6  Hart,7  Lakin,8 
and  others.  In  Hart's  two  cases  the  complicated  mixed  structure  of 
the  growth  justified  the  term  "  Adeno-fibro-lipo-chondroma  myxo- 
matosum." 

Dermoid  cysts,  primary  in  the  lung,  occur  only  in  very  rare  instances. 
They  are  more  common,  but  still  rare,  as  mediastinal  growths  which 
in  their  development  may  encroach  upon  or  develop  at  the  expense  of 
the  pulmonary  space.  Atelectasis,  venous  thrombosis,  and  dislocation 
of  the  heart  have  been  observed.  Degenerative  changes  in  the  cyst 
may  lead  to  inflammation  in  its  neighborhood.    Perforation  into  the 

1  Zeit.  f.  Krebs-Forschung,  1909-10,  vol..  viii. 

2  Die  krankhaften  Geschwulste,  Bd.  ii,  p.  102. 

3  Ein  Fall  von  diffuser  Knochenbildungen  in  der  Lunge,  Virchow's  Arch.,  1885,  ci,  156. 

4  Arch.  f.  Heilkunde,  1861,  Bd.  ii. 

6  Die  krankhaften  Geschwulste,  Berlin,  1863,  Bd.  i. 

6  Virchow's  Arch.,  1877,  Bd.  lxix. 

7  Die  primaren  Enchondrome  der  Lunge,  Zeit.  f.  Krebs-Forschung,  1906,  vol.  iv. 

8  Arch.  Middlesex  Hosp.,  1912,  xxv,  37. 


428  DISEASES  OF  THE  LUNGS 

lung  and  communication  with  branches  of  the  bronchial  system  was 
noted  in  11  of  the  44  cases  collected  by  Dangschat.1  Coincident 
cavity  formation  in  the  lung  may  or  may  not  exist.  The  disease  may 
occur  at  any  age,  but  is  more  common  before  thirty.  It  is  slowly 
progressive,  lasting  usually  over  two  years.  A  duration  of  five,  ten, 
twenty  and  even  more  than  forty  years  has  been  observed.  The 
finding  of  hairs  in  the  sputum  is  the  most  important  diagnostic  feature. 
These  may  persist  for  many  years.  The  symptoms  and  physical 
signs  do  not  differ  essentially  from  those  with  mediastinal  or  pul- 
monary tumors  from  other  causes.  Local  prominence  of  the  chest, 
in  which  at  times  fluctuation  may  be  determined,  is  important.  Extir- 
pation or  drainage  is  the  only  successful  treatment.  Katase2  reports 
an  instance  of  teratoma  of  the  lung,  and  finds  six  other  cases  in  the 
literature. 


MALIGNANT    TUMORS    OF    THE   BRONCHI   AND   LUNG. 

Malignant  tumors  of  the  lung  are  usually  secondary,  rarely  primary. 
The  primary  tumors  may  be  cancer  or  sarcoma.  Adler3  has  written 
at  length  on  this  subject  and  reviews  the  literature. 

Primary  Cancer  of  the  Lung. — Incidence. — In  the  combined  statis- 
tics of  Reinhard/  Fuchs,5  Wolf,6  Passler/and  Frohlich8  among  46,169 
autopsies  primary  cancer  was  found  in  only  105  (0.22  per  cent.)  or 
once  in  about  every  500  sections.  Among  1000  malignant  tumors 
(870  cancer,  130  sarcoma),  analyzed  by  Passler,  were  16  cases  of 
cancer  and  4  of  sarcoma  primary  in  the  lung,  thus  indicating  an  inci- 
dence of  1.6  per  cent,  of  all  malignant  tumors  and  1.83  per  cent,  of 
all  cancers  for  primary  cancer  of  the  lung. 

Etiology. — The  cause  of  cancer  of  the  lung  is  as  little  known  as  that 
of  similar  growths  elsewhere.  Trauma  has  been  thought  to  induce 
the  disease,  and  a  history  of  injury  to  the  chest  can  be  obtained  in  a 
certain  number  of  cases,  but  their  proportion  is  too  small  to  suggest 
that  this  is  a  significant  factor.  It  is  possible  that  more  importance 
may  be  ascribed  to  local  irritation.  The  coincidence  of  pulmonary 
cancer  and  tuberculosis  has  not  infrequently  been  observed.  Thus 
Wolf9  found  13  of  31  cases  of  primary  pulmonary  cancer  complicated 
with  tuberculosis,  which  he  was  disposed  to  regard  as  a  probable 

1  Beitriige  zur  klinischen  Chirurgie,  Tubingen,  1903,  vol.  xxxviii. 

2  Cent.  f.  allg.  Path.  u.  path.  Anat.,  1912,  xxiii,  146. 

3  Primary  Malignant  Growths  of  the  Lungs  and  Bronchi,  Longmans,  Green  &  Co., 
1912. 

4  Der  primare  Lungenkrebs,  Arch.  f.  Heilk.,  1878,  xix,  369.  Cancer  and  sarcoma 
are  not  differentiated  by  Reinhard. 

6  Beitrage  z.  Kenntniss  der  Geschwulstbildungcn  in  der  Lunge,  Diss.  Miinchen,  1886. 

6  Die  primare  Lungenkrebs,  Fortsch  der  Medicin,  1895,  No.  18,  Bd.  xiii,  p.  725. 

7  Ueber  das  primare  Carcinom  der  Lunge,  Virchow's  Arch.,  1896,  cxlv,  191. 

8  Ueber  das  primare  Lungenkarzinoms,  Inaug.  Diss.,  Berlin,  1899. 

9  Fortschritte  der  Med.,  1895,  xiii,  725  and  765. 


TUMORS  OF  THE  BRONCHI  AND  LUNG  429 

cause  in  8  cases.  Lenhartz1  found  tuberculosis  in  3  of  14,  Domeny2 
in  4  of  10  cases  and  Watsuju3  in  3  of  6  cases.  Watsuju  found  meta- 
plasia of  the  ciliated  epithelium  in  the  region  of  the  larynx  (twice), 
the  trachea  (once),  and  the  bronchus  (twice)  into  flat  epithelium 
in  3  of  30  tuberculous  bodies  which  he  examined.  In  one  of  the  cases, 
he  noted  slight  proliferation  of  the  lowest  layers  of  cells  and  extension 
through  the  basement  membrane  of  isolated  cell  clusters.  In  rare 
instances,  carcinoma  has  been  found  developing  in  a  tuberculous 
cavity,  among  others  by  Friedlaiider,4  Schwalbe,5  Wolf  ,6  and  Perrone.7 
Previous  local  lesions,  such  as  simple,  tuberculous  or  syphilitic  ulcers 
in  the  region  of  the  primary  bronchi  or  their  branches,  extension  to 
the  bronchi  of  glandular  mediastinal  suppuration,  or  pigment  perfora- 
tion may  serve  as  predisposing  factors  in  the  development  of  bronchial 
cancer,  just  as  gastric  ulcer  or  gall-stones  is  occasionally  followed  by 
cancer  of  the  stomach  or  bile  passages. 

Males  are  more  frequently  affected.  Of  68  cases  in  Passler's  series, 
in  which  the  sex  was  known,  50  (73  per  cent.)  were  males.  It  is  unusual 
for  the  disease  to  develop  before  the  fortieth  year.  Only  6  of  66  cases 
were  under  forty,  while  27  were  sixty  or  over. 

Pathology. — In  general,  the  right  lung  appears  to  be  more  often 
involved.  In  Passler's  series,  the  region  of  the  tracheal  bifurcation 
was  affected  in  5  cases,  the  disease  extending  thence  into  the  left 
primary  bronchus  in  one,  into  the  right  in  two  instances.  The  right 
lung  was  the  site  of  the  growth  in  35,  the  left  in  24  and  both  in  9  cases. 
None  of  the  lobes  can  be  regarded  as  specially  disposed  to  cancer. 
The  upper  and  lower  lobes  are  subject  to  the  development  of  primary 
growths  with  about  equal  frequency.  Involvement  of  the  apex  may 
be  observed,  as  in  Kasem-Beck's8  and  Schroder's9  cases. 

The  gross  appearance  is  very  variable,  but  a  relation  with  the 
bronchial  system  is  a  striking  feature  in  a  large  proportion  of  cases. 
A  single,  small,  rounded  tumor  mass  may  in  rare  instances  be  found 
projecting  into  one  of  the  larger  or  smaller  bronchi,  and  partially  or 
wholly  occluding  its  lumen.  In  one  of  the  Massachusetts  General 
Hospital  cases  (Autopsy  984),  a  circumscribed,  spherical  carcinoma 
about  1  cm.  in  diameter,  was  discovered  in  the  lower  part  of  the 
upper  lobe  of  the  right  lung.  This  was  found  on  microscopic  examina- 
tion to  occupy  the  lumen  of  a  small  bronchus  and  to  be  made  up  prin- 
cipally of  cuboidal  and  columnar  cells,  in  places  forming  imperfect 
tubules  and  apparently  taking  its  origin  from  the  bronchial  mucous 

1  Ebstein  and  Schwalbe,  Handbuch  der  prakt.  Med.,  1899. 

2  Zeit.  f.  Heilkunde,  1902,  Bd.  xxiii,  Abt.  f.  path.  Anat.,  H.  4. 

3  Zeit.  f.  Krebs-Forschung,  1904,  i,  445. 

4  Cancroid  in  einer  Lungenkaverne  Fort.  d.  Med.,  1885,  Bd.  hi,  No.  10,  Ref. 

5  Entwickelung  eines  primiiren  Karzinoms  in  einer  tub.  Kaverne,  Virchow's  Arch., 
cxlix.  329. 

6  Loc.  cit. 

7  Cancroid  in  einer  tub.  Lungenkav.  in  Orth  Festschrift,  Berlin,  1906. 
s  Zentralbl.  f.  innere  Med.,  No.  12,  1908. 

9  Deut.  Aerzte-Zeit.,  Berlin,  1906,  p.  313. 


430 


DISEASES  OE  THE  LUNGS 


glands.  Some  tumor  cells  could  be  seen  infiltrating  the  neighboring 
alveoli,  but  no  metastases  were  found.  The  new  growth  is  seldom 
discovered  at  such  an  early  stage.  In  a  second  case  (Autopsy 
2503,  see  Fig.  70),  a  small  tumor  projecting  into  the  bronchial  lumen 
had  already  metastasized  with  a  neighboring  gland.  It  is  more 
common  in  this  predominant  bronchial  group  to  find  that  the  primary 
growth  infiltrates  the  bronchial  wall  and  encroaches  on  its  lumen  for 
a  considerable  distance.  The  projection  into  the  bronchial  lumen  may 
be  intact  or  ulcerated.  Extension  of  the  tumor  is  likely  to  take  place 
by  way  of  the  bronchial  wall  and  to  outline  the  bronchial  divisions 
as  it  spreads  from  its  point  of  origin.  In  places,  the  radial  arrangement 
is  less  striking,  and  the  pulmonary  parenchyma  is  also  invaded  to  a 
greater  or  less  extent.  Small  or  large,  discrete  or  confluent  tumor 
nodules  or  masses  may  thus  arise,  many  or  few  of  which  may  be  seen 
to  surround  the  bronchi.  In  a  small  proportion  of  the  cases,  the 
bronchi  appear  to  take  only  an  insignificant  part  in  the  process,  and 

Fig.  70 


Carcinoma  (a)  of  bronchus  with  metastasis  into  neighboring  lymph  gland  (6)  (actual 
size).     (Dr.  Oscar  Richardson.) 

the  pulmonary  parenchyma  is  predominantly  affected.  The  new 
growth  is  usually  white,  grayish  or  grayish-yellow  in  color,  and  hard 
or  firm  in  consistency.  Dense,  resistant  masses  are  more  especially 
to  be  found  at  the  root  of  the  lung.  Primary  or  secondary  tumors 
developing  within  the  lung  substance  may  be  softer  and  even  marrow- 
like  in  character.  Secondary  degenerative  changes  are  not  uncommon. 
Fatty  degeneration,  softening  and  ulceration  of  the  centre  of  a  growth 
communicating  with  the  bronchi  may  result  in  the  formation  of 
cavities,  with  irregular,  shreddy  walls.  Infection  through  the  bronchi 
is  in  part  responsible  for  regressive  changes.  Hemorrhage  from  the 
eroded  surface  is  common. 

The  condition  of  those  parts  of  the  lungs  unaffected  by  the  new 
growth  is  variable.  In  some  instances  there  are  no  noteworthy  changes. 
There  may  be  emphysema.  Atelectasis  may  occur  in  compressed 
regions.  Acute  inflammatory  processes,  bronchopneumonia,  less 
often  lobar  pneumonia,  abscess,  and  gangrene  may  complicate  the 
disease.     Chronic  pulmonary  lesions  of  a  tuberculous  or  non-tuber- 


TUMORS  OF  THE  BRONCHI  AND  LUNG  431 

culous  character,  may  be  found.  They  may  precede  or  follow  the 
new  growth.  Partial  occlusion  of  a  bronchus  may  give  rise  to  stagna- 
tion of  secretion  beyond  the  site  of  the  obstruction.  Infection  of  the 
bronchial  wall  and  the  lung  may  then  lead  to  bronchiectasis,  single 
or  multiple  pulmonary  abscesses  and  interstitial  pneumonia.  Bac- 
terial or  cancerous  invasion  of  the  pleura  may  cause  adhesive,  fibrinous, 
serofibrinous,  hemorrhagic  or  purulent  pleurisy.  Pneumothorax  is 
observed  only  in  rare  instances. 

Metastases  were  absent  in  only  1 1  of  74  cases  analyzed  by  Passler. 
In  the  remaining  63  cases,  the  regional  lymph  glands  were  the  most 
common  site  of  secondary  deposits  and  were  affected  in  40.  The 
lung  was  secondarily  involved  in  31,  the  liver  in  23,  the  pleura  in  19, 
the  bones  in  12  and  distant  lymph  glands  and  the  kidney  in  8  each, 
while  the  larger  vessels  of  the  thoracic  cavity  (the  vense  cavse,  pul- 
monary arteries  and  veins)  in  an  equal  number.  The  spleen  and 
adrenal  were  each  involved  in  6  instances.  Metastases  may  occur  in 
almost  any  region  of  the  body.  Among  the  remaining  regions,  metas- 
tases in  the  brain  in  5  and  the  skin  in  2  cases  may  be  mentioned. 
Metastases  in  the  mediastinal  lymph  glands  may  give  rise  to  compres- 
sion or  thrombosis  of  the  mediastinal  veins,  with  resulting  stasis,  and 
to  compression  and  invasion  of  the  esophagus,  trachea,  and  recurrent 
laryngeal  nerves.  The  new  growth  may  invade  the  heart  muscle  or 
the  pericardium.  An  exudative  pericarditis  may  result.  Extension 
through  the  intervertebral  foramina  into  the  spinal  canal  has  caused 
transverse  myelitis. 

On  microscopic  examination,  cylindrical-celled  cancer  is  the  pre- 
vailing type,  but  polyhedral  cells  are  usually  also  found  to  compose  a 
variable  proportion  of  the  cells,  and  may  predominate  in  the  sections. 
Flat-celled  epithelial  cancer  is  less  commonly  observed.  In  this  group, 
cornification  is  occasionally  seen. 

Concerning  the  histogenesis  of  pulmonary  cancer,  much  difference 
of  opinion  has  prevailed,  and  the  question  cannot  yet  be  regarded  as 
settled.  The  appearance  and  arrangement  of  the  cells  in  the  cylin- 
drical-celled cancer  suggest  its  origin  from  the  epithelium  of  the 
bronchial  mucous  membrane  or  the  bronchial  mucous  glands.  An 
origin  from  the  bronchi  appears  to  be  sufficiently  established  by  the 
occcasional  finding  of  small  tumors  within  and  not  exceeding  the  limits 
of  the  bronchial  structures,  and  the  special  disposition  of  a  large 
majority  of  all  primary  lung  cancers  to  develop  in  or  along  the  bronchi 
or  their  divisions.  The  predominance  of  the  cylindrical-celled  type 
of  cancer  is  still  further  confirmation  of  such  an  origin.  Among 
Passler's  series  of  54  cases,  the  primary  source  appeared  to  be  the 
bronchi  in  at  least  47  (87  per  cent.).  The  histogenesis  of  the  flat- 
celled  epithelial  cancer  is  less  clear.  This  form  may  be  regarded  as 
taking  its  origin  from  the  alveolar  or  the  bronchial  epithelium  by 
a  process  of  metaplasia.  The  morphologic  similarity  between  flat 
epithelial  cancer  cells  and  alveolar  epithelium  may  be  urged  in  support 


432  DISEASES  OF  THE  LUNGS 

of  an  origin  from  the  alveoli,  while  the  finding  of  apparent  transitions 
from  normal  cylindrical  bronchial  epithelium  to  flat  cancer  cells, 
the  occasional  presence  of  cornification  and  epithelial  perles  may  be 
urged  in  favor  of  a  bronchial  origin. 

The  spread  of  cancer  of  the  lung,  as  was  first  shown  by  Stilling,1 
takes  place  principally  by  way  of  the  lymph  vessels  in  the  walls  of 
the  bronchi  and  the  bloodvessels,  and  by  way  of  the  bronchi  them- 
selves. A  cancer  primary  in  the  wall  of  a  bronchus  invades  and 
further  develops  within  its  lumen,  through  which  it  finds  its  way  into 
the  pulmonary  alveoli.  Extension  by  continuity  is  probably  unneces- 
sary and,  as  Passler  has  suggested,  tumor  particles  may  be  carried 
by  aspiration  from  the  region  of  the  hilus  of  the  lung  to  the  finer 
branches  of  the  bronchi,  where  they  lead  to  secondary  nodules 
apparently  developing  in  the  pulmonary  parenchyma.  Pulmonary 
cancer  appears  to  enlarge  by  proliferation  of  cells  composing  the 
tumor  itself  (central  growth)  rather  than  by  the  transformation  of 
peripheral  and  non-cancerous  into  cancer  cells  (peripheral  growth). 

Lymphatic  invasion,  with  extension  to  the  bronchial  and  medias- 
tinal lymph  glands,  takes  place  after  a  certain  period  in  the  develop- 
ment of  all  pulmonary  cancers.  In  rare  instances,  however,  cancerous 
lymphangitis,  involving  a  part  or  the  whole  of  one  lobe  or  of  one  or 
both  lungs,  becomes  so  striking  a  feature  as  to  justify  the  term  mil i wry 
carcinosis.  When  the  subpleural  lymphatics  are  affected,  they  may 
appear  as  a  coarse  grayish-white  network,  on  the  surface  of  the  lung, 
outlining  the  perilobular,  periacinous,  and  perialveolar  lymphatics. 
On  cross  section,  the  injected  pulmonary  lymph  vessels  appear  as 
fine,  miliary,  grayish  granulations  which  may  be  readily  overlooked 
or  confused  with  miliary  tubercles,  their  true  nature  at  times  first 
becoming  apparent  on  microscopic  examination.  Larger  or  smaller 
nodules  or  masses  of  cancer  may  be  associated.  Pulmonary  carcinosis 
is  more  commonly  observed  in  secondary  than  in  primary  lung  cancer. 
When  generalized,  it  may  arise  by  retrograde  infection  of  the  lung 
from  the  mediastinal  glands,  as  suggested  by  Girode.2 

Primary  Sarcoma  of  the  Lung. — This  is  much  less  common.  The 
following  report  is  based  on  42  cases3  of  certain  or  probable  primary 
sarcoma. 

1  Ueber  primaren  Krebs  der  Bronchien  und  dos  Lungenparenchyms,  Virchow's  Arch., 
Bd.  lxxxiii,  p.  77. 

2  Lymphangite  cancereuse  pleuropulmonaire  sans  cancer  du  poumon.,  Arch.  gen.  de 
med.,  Janv.,  1889. 

3  Poisson  et  Robin.  (Gaz.  med.  de  Paris,  1856,  No.  9.)  Demange.  (Rev.  Med.  de 
l'Est.,  Aout,  1875.)  Chiari.  (Anz.  d.  Gesellschaft  der  Aerzte  in  Wien,  1878,  No.  6.) 
Reinhard.  (Arch.  d.  Heilkunde,  1878,  vol.  xix,  second  case.)  Weichselbaum.  (Vir- 
chow's Arch.,  Bd.  lxxxv,  p.  559.)  Blumenthal.  (Primare  maligne  Lungentumoren, 
Inaug.  Diss.,  Berlin,  1881.)  Rutimeier.  (Korrespondenzbl.  f.  Schw.  Aerzte,  1885,  p. 
576.)  Fuchs.  (Inaug.  Diss.,  Miinchen,  1886);  two  cases  (I  and  II).  Hildebrand. 
(Zwei  Fiille  von  primaren  malignen  Lungentumoren  im  Anschluss  an  Tuberkulose, 
Inaug.  Diss.,  Marburg,  1887.)  Origin  from  lung  or  bronchial  lymph  glands  somewhat 
doubtful.  Schech.  (Deut.  Arch.  f.  klin.  Med.,  1890-91,  xlvii,  411.)  Spillmann  and 
Haushalter.      (Gaz.  hebd.  de  med.  et  chir.,  December  5,  1891.)  Thought  to  originate  in 


TUMORS  OF  THE  BRONCHI  AND  LUNG  4'4'4 

Etiology.  —  Etiologic  factors  are  uncertain.  The  ages  of  the 
reported  cases  vary  from  three  to  seventy-eight  years.  Sarcoma  is 
much  more  common  at  an  early  age  than  cancer.  In  the  first  decade, 
only  two  cases  are  recorded.  .  Two  cases  were  from  ten  to  twenty, 
9  from  twenty  to  thirty,  5  from  thirty  to  forty,  5  from  forty  to  fifty, 
six  from  fifty  to  sixty,  4  from  sixty  to  seventy,  and  5  from  seventy  to 
eighty.  Thus  in  this  series,  nearly  two-thirds  were  under  forty.  Males 
are  more  commonly  affected,  numbering  25  of  the  38  cases  in  which 
the  sex  is  given. 

A  remarkable  endemic  malignant  disease  of  the  lungs  is  described  by 
Harting  and  Hesse1  among  the  workers  in  the  Schneeberger  mines. 
Of  about  an  average  number  of  650  men  employed,  63  were  affected 
between  1869  and  1871,  47  from  1872  to  1874,  and  40  from  1875  to 
1877.  About  75  per  cent,  of  the  deaths  from  all  causes  were  due  to 
this.  The  disease  should  be  classed  not  as  carcinoma,  but  as  lympho- 
sarcoma, and  appeared  to  take  its  origin  from  the  bronchial  lymph 
glands.  Its  earliest  appearance  was  after  twenty  years,  rarely  after 
fifty  years  of  service  in  the  mines.  The  cutters  were  earliest  affected. 
The  disease  is  ascribed  to  the  irritating  effect  of  inhaled  arsenic  in 
combination  with  cobalt.  Arnstein2  reports  as  the  result  of  the 
examination  of  postmortem  material  from  two  cases  that  the  condition 
in  one  proved  to  be  chronic  tuberculosis  and  in  the  other  pulmonary 
carcinoma,  in  many  places  showing  a  sarcoma-like  structure.  Of 
three  other  cases  reported  to  him  by  Schmorl,  one  proved  to  be  pave- 
ment-celled carcinoma,  and  the  two  remaining  cases  round-celled 
sarcoma. 

Pathology. — Pulmonary  sarcoma  usually  occurs  as  small  or  large 
multiple  and  isolated  or  solitary  tumors,  varying  in  size  from  a  hen's 

the  lung  but  may  have  come  from  the  pleura.  Braureuter.  (Inaug.  Diss.,  Miinchen, 
1891.)  Origin  from  bronchial  lymph  gland  at  the  root  of  the  lung.  Vandervelde. 
(Jour,  de  med.  chir.  et  Pharmacol.,  Brux.,  1892,  xciv,  193.)  Ranglaret.  (Bull.  soc. 
anat.,  1893,  p.  591.)  Origin  undertain.  Raymond.  (Ibid.)  Ferrand.  (Bull,  et  mem. 
soc.  med.  d'hop.  de  Paris,  1893,  s.  S,  x,  796.)  Habershon.  (Trans.  Path.  Soc,  London, 
1897,  8,  xlix,  17.)  Pollak.  (Ein  Fall  von  prim.  Lungensarkom.,  Inaug.  Diss.,  Wiirz- 
burg,  1897.)  Milian  et  Bernard.  (Bull.  soc.  anat.,  1898.)  Hellendahl.  (Zeit.  f.  klin. 
Med.,  1899,  Bd.  xxxvii.)  Schnick.  (Inaug.  Diss.,  Greifswald,  1899.)  Meyer.  (Beitrag 
zur  Casuistik  der  prim.  Lungensarugcome,  Ina.  Diss.,  Miinchen,  1900.)  Milian  et 
Maute.  (Bull.  soc.  anat.,  Janvier,  1901.)  Lewit.  (Inaug.  Diss.,  Erlangen,  1901.) 
Baumann  and  Bainbridge.  (Trans.  Path.  Soc,  London,  1902-03,  liv,  150.)  Rolleston 
and  Trevor.  (British  Med.  Jour.,  1903,  i,  361.)  Clement.  (Lyon  med.,  1904,  cii,  630.) 
Kobylinski.  (Ueber  prim.  Sarkome  in  der  Lunge,  Inaug.  Diss.,  Greifswa!d,  1904.)  Two 
cases.  Roth.  (Ueber  primares  Lungensarkom.  mit  einem  kasuistischen  Beitrag,  Inaug. 
Diss.,  Miinchen,  1904.)  Broc  (Bull,  et  mem.  Soc.  anat.  de  Paris,  1905,  lxxx,  90.) 
Schmidt.  (Cor.-Bl.  f.  Schw.  Aerzte,  Basel,  1905,  xxxv,  53-55.)  Pater  et  Rivet,  (Arch, 
de  med.  exp.  et  d'anat.  path.,  Paris,  1906,  xviii,  85-101.)  Eckersdorff.  (Centralbl.  f. 
allg.  Path.  u.  path.  Anat,,  1906,  xvii,  355.)  Two  cases.  Delporte  et  Guibal.  (Arch,  de 
med.  et  pharm.  mil.,  Paris,  1907,  i,  286.)  Curl.  (British  Med.  Jour.,  1908,  i,  1408.) 
Lehndorff.  (Wien.  med.  Woch.,  1909,  xxii,  1053.)  Boschowsky.  (Frankfurter  Zeit,  f. 
Path.,  1911-12,  ix,  239.)  Steven.  (Amer.  Jour.  Med.  Sci.,  1912,  cxliv,  193.)  Berge 
et  R.  J.  Weissenbach.     (Bull,  et  Mem.  d.  la  soc.  Anat.  d.  Paris,  1912,  Ixxxvii,  210.) 

1  Der  Lungenkrebs,  die  Bergkrankheit  in  den  Schneeberger  Gruben,  Vierteljahr- 
schrift  fur  Gerichtliche  Medicin  und  offentliches  Sanitatswesen,  1879,  xxx  u.  xxxi,  296. 

2  Verhandl.  d.  deut.  path.  Gesellsch.,  1913,  xvi,  332. 

28 


434  DISEASES  OF  THE  LUNGS 

egg  to  an  infant's  head.  The  large,  single  tumors  arc  somewhat  more 
common.  In  some  instances,  a  diffuse  growth  uniformly  infiltrates 
the  tissue.  The  disease  is  more  common  on  the  left  side  as  in  24  of 
this  series.  The  right  side  was  involved  in  14,  both  lungs  in  4  cases. 
The  disease  shows  no  striking  disposition  to  invade  one  lobe  more 
than  another.  A  location  in  the  left  lower  or  right  upper  lobe,  singly 
or  combined  with  other  regions,  was  somewhat  more  common  than 
elsewhere.  The  tumors  are  rather  soft  than  hard,  and  of  a  whitish, 
grayish,  or  reddish  color.  Metastases  are  found  in  the  lung,  the  bron- 
chial, mediastinal,  or  other  glands.  The  bronchial  and  mediastinal 
glands  are  most  often  affected,  but  secondary  deposits  may  be  found 
in  any  organ  of  the  body.  In  general  it  may  be  said  that  metastases 
appear  to  be  less  common  with  pulmonary  sarcoma  than  with  cancer, 
while  growth  by  extension  is  more  frequent.  In  rare  instances,  the 
sternum,  ribs  or  vertebrae  are  eroded.  Fatty  degeneration,  suppura- 
tion, and  cavity  formation  are  not  infrequently  observed.  Calcification 
and  ossification  of  a  part  of  the  tumor  is  occasionally  seen.  Complicat- 
ing lesions  in  the  lung,  the  pleura  and  other  nearby  or  remote  organs 
do  not  differ  essentially  from  those  with  pulmonary  cancer. 

Various  histologic  types  of  sarcoma  are  represented  in  the  pul- 
monary form  of  the  disease.  Round-celled  sarcoma  is  more  common 
than  other  forms.  The  cells  may  be  small  or  large.  Spindle-celled 
sarcoma  stands  next  in  frequency.  Giant-celled,  lympho-,  myxo- 
and  fibrosarcoma  are  occasionally  observed.  A  papillary  adeno- 
sarcoma  was  found  in  one  instance.  The  growth  probably  takes  its 
origin  from  the  peribronchial  lymphatic  or  connective  tissue. 

Symptoms. — The  clinical  features  of  pulmonary  cancer  and  sarcoma 
are  practically  the  same.  The  two  diseases  are  therefore  considered 
together  in  the  following  description. 

The  manifestations,  their  grouping  and  progress  are  so  variable  in 
different  cases  that  it  is  difficult  to  construct  a  typical  clinical  picture. 
In  a  number  of  the  cases,  however,  a  patient  in  previous  good  health 
begins  to  cough,  at  first  without  expectoration.  The  cough  is  con- 
stant and  harassing,  and  later  accompanied  by  a  scanty  mucoid  or 
mucopurulent  sputum  in  which  at  times  bloody  streaks  or  masses 
are  noted.  The  general  health  may  be  little  if  at  all  disturbed.  Sooner 
or  later,  there  is  dyspnea,  at  first  only  after  unusual  exertion,  but 
gradually  increasing  in  duration  and  intensity  until  it  becomes  constant 
and  distressing.  Pain  of  slight  degree  is  common,  and  is  usually 
referred  to  the  axillary  region,  but  may  be  felt  in  the  sternum,  shoulder 
or  abdomen.  It  is  seldom  a  prominent  feature.  A  troublesome  sense 
of  intrathoracic  discomfort  or  pressure  is  frequent.  With  the  prog- 
ress of  the  disease  the  general  condition  suffers.  Loss  of  weight  and 
strength  may  be  progressive.  The  appetite  fails.  Cough  and  dyspnea 
may  become  paroxysmal.  Orthopnea  is  not  infrequent.  Night  sweats 
are  uncommon.  Death  may  take  place  from  asthenia,  in  an  attack 
of  suffocation,  from  hemorrhage,  a  complicating  infection,  or  metastases. 


TUMORS  OF  THE  BRONCHI  AND  LUNG  435 

Cough  is  usually  an  early  symptom,  but  may  be  absent  throughout 
in  rare  instances.  Dyspnea  may  be  the  first  symptom  and  is  usually 
a  prominent  and  progressive  feature.  It  is  more  troublesome  with 
rapidly  growing  tumors,  those  complicated  by  pleural  effusion,  or 
when  the  new  growth  compresses  or  invades  the  trachea  or  larger 
bronchi.    Involvement  of  the  larger  tubes  may  cause  stridor. 

Pain  is  common,  but  not  usually  severe  unless  the  pleura  is  involved. 
It  may  then  be  intense.  Fever  of  an  irregular  or  intermittent  type  may 
be  present,  and  was  noted  in  19  of  Frankel's1  35  cases  of  malignant 
lung  tumor.  It  may  be  due  to  secondary  infection  or  absorption  of 
toxic  material.  In  a  small  proportion  of  the  cases  there  are  important 
localizing  symptoms  referable  to  extension  or  metastasis  into  the 
mediastinum.  Compression  of  the  esophagus  or  recurrent  laryngeal 
nerve  may  cause  dysphagia  or  hoarseness.  Involvement  of  the  vagus, 
the  phrenic  or  sympathetic  nerves  is  also  probable,  but  is  thus  far 
not  indicated  in  the  clinical  histories  of  the  reported  cases.  Exten- 
sion to  the  spinal  cord  through  the  intervertebral  foramina  may  cause 
transverse  myelitis.  Symptoms  referable  to  metastases  in  other  organs, 
as  in  the  brain,  may  in  rare  instances  complicate  the  clinical  picture. 
If  cerebral  symptoms  are  an  early  feature  they  may  mask  the  pul- 
monary disease,  as  in  Passler's2  patient,  a  man  aged  sixty-three  years, 
who  had  right-sided  hemiplegia.  His  pulmonary  symptoms  were 
regarded  during  life  as  postapoplectic,  but  proved  at  postmortem 
examination  to  be  due  to  primary  lung  cancer.  The  cerebral  lesions 
were  metastatic. 

Physical  Signs. — In  general,  the  cases  may  be  divided  roughly  into 
two  groups.  In  the  first  and  larger  group,  the  physical  signs  are  for 
the  most  part  referable  to  the  lung  within  which  the  disease  develops, 
extending  peripherally  toward  the  pulmonary  surface,  at  times  into 
the  pleura.  In  the  second  and  smaller  group,  the  root  of  the  lung  is 
primarily  affected,  the  disease  extending  thence  into  the  lung,  the 
mediastinal  glands  or  both.  In  this  class,  the  physical  signs  are  prin- 
cipally due  to  the  enlarged  mediastinal  glands. 

In  the  pulmonary  formoi  the  disease,  examination  of  the  lungs  may 
be  negative,  if  the  tumor  is  centrally  placed.  Unequal  respiratory 
motion  of  the  two  sides  of  the  chest  may  be  observed.  Over  the  site 
of  a  process  which  reaches  the  periphery  or  secondarily  involves  the 
pleura,  the  intercostal  spaces  may  be  narrowed  or  fuller  and  wider 
than  normal.  There  is  dulness  or  flatness,  a  sense  of  resistance, 
diminished  or  absent  tactile  fremitus,  voice  and  whispered  sounds, 
and  respiratory  murmur.    Rales  are  absent  in  uncomplicated  cases. 

New  growths  at  the  root  of  the  lung,  with  extension  or  metastasis 
to  the  mediastinum  may  be  indicated  by  dulness  over  and  for  a 
variable  but  usually  only  short  distance  to  either  side  of  the  upper 
sternal  region  in  front  and  the  upper  dorsal  spines  behind.    Atypical 

1  Spec.  Path.  u.  Ther.  der  Lungenkrankheiten,  1904.  2  Loc.  cit.,  Case  III. 


436  DISEASES  OF  THE  LUNGS 

murmurs  due  to  compression  of  the  great  mediastinal  vessels  may 
occasionally  be  heard.  Partial  occlusion  of  a  main  bronchus  may 
be  suggested  by  the  presence  of  a  peculiar  bronchial  murmur,  heard 
to  one  or  the  other  side  of  the  spinal  column  at  the  level  of  the  hilus 
of  the  lung,  and  due  to  narrowing  of  the  air  current  as  it  passes  the 
obstruction.  It  is  spoken  of  by  the  French  as  "Cornage."  An  inter- 
esting variation  in  the  physical  signs  on  the  part  of  the  lung  may  be 
suggestive.  Dulness  or  dull  tympany,  with  faint  bronchial  or  absent 
breathing,  discovered  over  a  certain  pulmonary  territory,  may  change 
its  degree  and  extent  from  time  to  time,  as  in  the  cases  described  by 
Grunwald,1  Frankel  and  others.  The  dulness  and  diminished  breath- 
ing are  due  to  occlusion  of  a  bronchus  supplying  the  affected  region, 
with  consequent  atelectesis  of  the  lung.  Relief  of  the  obstruction 
through  ulceration  of  the  tumor  mass  or  eccentric  pull  of  contracting 
connective  tissue  may  be  followed  by  the  reentry  of  air  and  inflation 
of  the  lung.  The  repeated  closing  and  opening  of  the  bronchus  are 
followed  by  the  appearance,  modification  or  disappearance  of  the 
signs. 

Inequalities  of  the  radial  pulses  may  be  determined.  Tracheal  tug 
may  be  demonstrated,  but  less  often  than  with  aortic  aneurism.  It 
may  be  due  to  transmission  of  pulsations  from  the  aorta  to  a  primary 
bronchus  through  an  intervening  and  enlarged  gland,  as  in  Auer- 
bach's2  case,  with  metastases  into  the  mediastinum  from  a  carcinoma 
of  the  stomach.  Adhesions  between  the  aorta  and  the  trachea  or 
bronchi  in  consequence  of  glandular  involvement  may  likewise  be  a 
cause.  Thoracic  pulsation  may  occasionally  be  observed,  especially 
in  the  upper  sternal  region.  It  is  usually  due  to  transmission  of 
impulses  from  the  aorta  to  a  tumor  mass  in  apposition  with  it  and  the 
chest  wall. 

Dilatation  of  the  superficial  veins  is  not  uncommon.  It  may  be 
due  to  compression  or  thrombosis  of  the  mediastinal  vessels.  The 
venous  dilatation  is  usually  limited  to  the  upper  sternal  and  cervical 
region  and  may  occur  on  one  or  both  sides.  The  veins  of  the  shoulder 
or  upper  abdomen  may  also  be  involved.  Edema  of  the  chest  wall 
over  the  site  of  the  new  growth  is  occasionally  seen.  In  Reinhard's 
case,  the  temporal  veins  wrere  tortuous;  the  face,  neck,  arms  and 
thorax  as  far  as  the  attachment  of  the  diaphragm  wTere  edematous. 
Cyanosis  may  also  be  noted.  The  heart  may  be  displaced  by  a  pul- 
monary or  pleural  tumor,  with  or  without  the  presence  of  pleural  fluid. 

Metastases  and  cachexia  are  common  to  a  certain  proportion  of 
both  types  of  the  disease.  Metastases  may  occur  in  any  part  of  the 
body,  but  in  accessible  regions  in  only  a  small  number  of  the  cases. 
Palpably  enlarged  lymph  glands  were  noted  in  8  (18.6  per  cent.)  of 
43  cases  collected  by  Angeloff.3  Glandular  invasion  may  affect  the 
supraclavicular,  the  cervical  or  axillary  glands.    The  left  supraclavi- 

1  Munch,  mod.  Woch.,  1889,  p.  548.  2  Deut.  mod.  Wooh.,  1900,  No.  8. 

3  Ueber  das  primare  Lungencarcinom  Inaug.  Diss.,  Miinchen,  1905,  p.  46. 


TUMORS  OF  THE  BRONCHI  AND  LUNG  437 

cular  group  are  somewhat  more  often  involved.  General  adenopathy 
may  be  seen  in  rare  instances,  as  in  Pater  and  Rivet's  case  of  primary 
lung  sarcoma.  Cachexia  may  develop  early  or  late,  at  times  not  at 
all  in  the  course  of  the  disease. 

Sputum  may  be  absent.  When  present,  it  is  very  variable  in 
character  and  without  distinctive  features  on  macroscopic  exami- 
nation. It  is  usually  scanty,  mucoid  or  mucopurulent.  An  abundant 
purulent  expectoration  is  occasionally  seen  in  the  later  stages  of  new 
growths  which  have  undergone  necrosis  and  cavity  formation.  In 
such  cases  it  may  be  foul.  Blood  is  present  in  the  sputum  in 
from  a  third  to  a  half  of  the  cases.  Repeated  small  amounts  in 
streaks  or  masses  are  more  common.  Intimate  admixture  with  blood 
may  give  the  sputum  a  rusty  color.  Gelatinous,  reddish  sputum 
resembling  currant  jelly  has  been  thought  distinctive  of  malignant 
tumor,  but  is  found  in  other  conditions.  It  is  present  in  only  a  small 
proportion  with  tumor.  V.  Criegern1  found  it  in  only  14  of  150 
cases  of  malignant  pulmonary  disease.  Frank  and  even  fatal  hemor- 
rhage may  occur.  In  one  of  Passler's2  cases,  hemoptysis  was  an  initial 
symptom  and  proved  fatal  in  the  last  of  three  attacks  on  successive 
days.  At  the  postmortem  examination,  it  was  found  that  a  carci- 
noma of  the  right  bronchus  had  eroded  a  branch  of  the  pulmonary 
artery. 

Tumor  fragments  have  been  found  in  the  sputum  from  cases  of 
primary  pulmonary  cancer  by  Claisse,3  Menetrier,4  and  Weininger;5 
primary  sarcoma  by  Feldt;6  secondary  cancer  by  Claisse,7  Troisier8 
and  Menetrier;9  and  secondary  sarcoma  by  Hampelm,10  Huber11  and 
P'eldt.12  They  are  more  likely  to  be  found  when  the  sputum  is  bloody 
and  are  probably  commoner  than  the  small  number  of  reported  cases 
indicate.  Secondary  infection  and  necrosis  of  the  tumor,  however, 
may  convert  them  into  a  conglomerate  mass  of  degenerated  cells  and 
debris  without  characteristic  structure.  The  search  is  more  likely 
to  be  successful  if  the  fresh  sputum,  mixed  with  normal  saline  solution, 
is  examined  in  a  flat  glass  dish  with  a  black  background  and  coherent 
balls  or  masses  carefully  teased  apart.  Bits  of  new  growth,  washed 
free  of  adherent  blood  and  mucus,  may  then  appear  as  reddish,  grayish 
or  whitish  particles  or  shreds.  In  Hampeln's  case  with  a  giant-celled 
sarcoma  of  the  lung  secondary  to  an  osteosarcoma  of  the  leg,  the 
pulmonary  growth  had  invaded  a  primary  bronchus,  and  masses  as 
large  as  5.5  cm.  long  and  2.5  cm.  thick  were  expectorated.  In  Feldt's 
case,  of  round-celled  sarcoma,  particles  scarcely  1  mm.  in  diameter 
satisfactorily    demonstrated    the    histologic    structure.      Suspected 

1  Akute  Bronchiektasie,  Leipzig,  1903,  p.  108.  2  Loc.  cit.,  Case  III. 

3  Soc.  med.  des  hop.,  January  6,  1899.  4  Ibid. 

5  Zeit.  f.  Heilkunde,  1901,  p.  78,  Case  II. 

6  Deut.  med.  Woch.,  July  9,  1903.  '  Loc.  cit. 
8  Ibid.  9  Ibid. 

10  St.  Petersburger  med.  Woch.,  1876,  No.  40. 

»  Zeit.  f.  klin.  Med.,  1890,  xvii,  341.  J2  Loc.  cit. 


438 


DISEASES  OF   THE  LUNGS 


material  should  be  hardened^  cut  and  stained  according  to  the  usual 
method. 

Fig.  71 


Fresh  sputum  from  a  case  of  malignant  disease  of  the  lung:  a,  large  mononuclear 
cell;  b  and  b,  polynuclear  cells;  d,  red-blood  corpuscles;  e,  fine  fat  drops;  /,  granular 
cell;  m,  large  cell  group.      X  275.      (Betschert.) 

Fig.   72 


., 

. 

'" 

!  -  "i 

- 

Fresh  sputum.    Malignant  disease  of  lung:    m,  cell  group.      X  275.     (Betschert.) 


Numerous  isolated  cells  or  cell  clusters  (Figs.  71  and  72)  may  also  be 
found  in  the  sputum  from  cases  with  pulmonary  carcinoma,  as  in  the 
cases    described    by     Hampeln;1    Japha,2     Betschert3     and    others. 

1  Petersburger  med.  Woch.,  1SS7,  Xo.  17,  and  Zeit.  f.  klin.  Med.,  32,  1897,  p.  247, 
q.  v.  for  a  discussion  of  tin-  subject. 

-  CFeber  prim.  Lungenkrebs,  Inaug.  Diss.,  Berlin,  1892. 
3  Virchow's  Arch.,  1895,  cxlii,  86. 


TUMORS  OF  TEE  BRONCHI  AND  LUNG 


439 


Hampeln  regards  a  sputum  composed  exclusively  or  for  the  most  part 
of  unpigmented,  polymorphous,  polygonal  cells  of  variable  size  and 
with  well-defined  nucleus  and  nucleolus,  isolated  and  in  clusters,  as 
distinctive  of  new  growth.  As  he  suggests,  the  normal  squamous 
cells  from  the  surface  of  the  mucous  membrane  of  the- mouth,  pharynx 
and  larynx,  the  small  polyhedral  or  cubical  cells  of  the  deeper  layers 
of  the  air  passages  and  the  polygonal  alveolar  epithelium  are  found 
only  in  rare  instances  in  the  sputum,  and  then  only  in  isolated 
examples.  Lenhartz1  ascribes  a  greater  diagnostic  importance  to  large, 
strongly  refractive  spherical  bodies  with  coarse  or  fine,  fatty  granules 
("Fettkornchenkugeln."  See  Fig.  73). 

Fig.  73 


Refractive  spherical  bodies  with  coarse  or  fine,  fatty  granules  "Fettkornchenkugeln" 

(Lenhartz.) 

Complications. — These  are  numerous  and  responsible  for  much  of 
the  complexity  in  the  clinical  picture.  Bronchitis  is  frequent  in  the 
neighborhood  of  the  new  growth  or  over  a  wider  area.  Ulceration 
with  consequent  cavity  formation  may  give  rise  to  an  abundant, 
purulent,  foul  sputum  mixed  with  blood.  Secondary  infection  of  the 
lung  may  cause  bronchopneumonia,  abscess,  gangrene,  and  pulmonary 
induration,  and  the  clinical  aspect  may  then  be  that  of  a  suppurative 
process  without  evidence  of  malignant  disease.  Partial  or  complete 
closure  of  a  bronchus  may  cause  bronchiectasis  beyond  the  point  of 
the  obstruction.  Atelectasis  may  likewise  be  a  consequence  and  result 
in  retraction  of  the  side,  dulness,  diminished  or  absent  respiratory 
murmur,  voice  and  tactile  fremitus  over  the  affected  region.     Such 


1  Ebstein-Schwalbe,  Handbuch  der  praktischen  Medizin,  2  Aufl.,  Bd.  iv,  p.  360. 


440  DISEASES  OF   THE  LUNGS 

signs  were  present  in  Korner's1  case  over  the  greater  part  of  the  right 
lung.  At  autopsy  the  right  primary  bronchus  was  found  obstructed. 
The  right  lung  was  completely  retracted  and  for  the  most  part  airless, 
but  without  inflammatory  changes.  Lobar  pneumonia  may  complicate 
the  disease  and  prove  fatal. 

Involvement  of  the  pleura  or  pericardium  is  not  uncommon. 
Pleurisy  pain  may  be  a  distressing  feature.  An  accumulation  of  fluid 
may  aggravate  the  dyspnea  and  obscure  the  signs  of  underlying  pul- 
monary disease.  Evident  pleural  exudate  which  gave  rise  to  more 
or  less  troublesome  symptoms  during  life  was  noted  in  8  of  the  02 
cases  of  primary  lung  cancer  collected  by  Angeloff.2  The  exudate 
was  serohemorrhagic  in  0,  serous  in  one,  and  purulent  in  the  last  case. 
Pneumothorax  has  not  been  observed. 

Metastatic  growths  in  regions  remote  from  the  lungs  may  lead  to 
disturbances  which  dominate  the  clinical  picture.  Intracranial  invasion 
may  cause  symptoms  of  meningitis,  cerebral  tumor  or  hemorrhage, 
the  secondary  nature  of  which  may  be  first  ascertained  at  autopsy. 

Diagnosis. — This  has  been  correctly  made  during  life  in  only  a  few 
instances.  The  rarity  of  the  disease,  the  consequent  failure  to  con- 
sider it  in  obscure  cases  and  the  readiness  with  which  it  may  be 
confused  with  more'  common  conditions  are  largely  responsible.  The 
finding  of  tumor  fragments  in  the  sputum  is  the  only  distinctive  sign. 
Of  especially  suggestive  features  may  be  mentioned  the  occurrence 
of  such  pulmonary  symptoms  as  have  been  described  in  a  patient 
past  forty,  without  a  family  history  of  tuberculosis  or  known  oppor- 
tunity for  contagion,  with  progressive  failure  of  health  and  strength, 
bloody  sputum,  absence  of  fever,  physical  signs  like  those  with  encysted 
pleural  effusion,  and  evidence  of  mediastinal  pressure.  In  addition, 
a  bronchial  murmur  heard  to  one  or  the  other  side  of  the  spinal 
column  over  the  lung  hilus  and  a  variation  in  the  physical  signs  sug- 
gestive of  successive  closure  and  opening  of  a  bronchus  may  be  of 
importance.  The  discovery  of  enlarged  glands  in  an  accessible  region 
and  a  negative  tuberculin  test  will  also  be  of  assistance.  The  age  of 
the  patient  has  a  certain  bearing  on  the  diagnosis,  inasmuch  as  cancer 
develops  before  the  fortieth  year  only  in  rare  instances,  while  sarcoma 
occurs  practically  at  any  age.  The  mueh  greater  frequency  of  primary 
cancer  may  be  taken  into  consideration,  unless  definite  evidence  of 
either  cancer  or  sarcoma  can  be  obtained. 

X-ray  Examination. — This  may  be  helpful  when  interpreted  in  the 
light  of  a  careful  clinical  investigation.  The  location  and  extent  of 
the  new  growth  in  the  lung  and  the  presence  of  metastases  in  the 
mediastinum  may  be  determined.  An  unexpected  central  lesion  may 
be  found.    The  absence  of  a  shadow  at  the  apex  when  an  upper  lobe 

1  Ein  Fall  von  priniarem  Krebs  der  grossen  Luftwege  mit  sieben  Wochen  lang  beste- 
hender  Obstruktionsatelektase  d.  ganz.  rechten  Lunge,  Munch,  mcd.  Woch.,  1888, 
No.  11. 

-  [Jeber  das  prim:irt>  Lungencarcinome,  Inaug.  Diss.,  Miinchen,  1905. 


TUMORS  OF  THE  BRONCHI  AND  LUNG' 


441 


is  involved  may  help  in  the  differentiation  between  tumor  and  tuber- 
culosis. It  is  especially  in  the  new  growths  taking  their  origin  from 
the  hilus  that  the  .r-rays  may  be  expected  to  be  of  most  value.  A  dense 
shadow  at  the  root  of  the  lung  with  radial  projections  along  the  course 
of  the  larger  bronchi  toward  the  periphery  is  suggestive  of  primary 
cancer.  Plates  taken  with  the  breath  held  in  full  inspiration  will  be 
found  most  satisfactory.  The  exposure  may  well  be  dorso ventral, 
ventrodorsal,  and  in  various  oblique  positions.  The  fluoroscopic 
screen  may  also  be  used. 

Fig.  74 


Metastatic  sarcoma.  Spindle-celled  sarcoma  removed  from  lumbar  region  six  years 
ago.  Operation  for  local  recurrence  two  years  ago.  Dense  shadow  occupying  greater 
part  of  left  side  of  chest.  At  right  base  two  small  nodules.  Upper  part  of  both  sides 
studded  with  small  nodules.    Displacement  of  the  heart  to  the  right.     (No.  186,393.) 


Exploratory  Puncture. — Positive  results  by  this  means  have  been 
obtained  by  Kronig1  in  a  case  of  primary  sarcoma,  and  Hellendahl2 
in  two  cases,  one  of  primary  and  the  other  of  secondary  sarcoma. 
When  in  doubt  as  to  the  presence  within  the  syringe  of  aspirated 

1  Diagnostischer  Beitrag  zur  Herz-  und  Lungenpathologie,  Berl.  klin.  Woch.,  1897, 
vol.  li. 

2  Ein  Beitrag  zur  Diagnostik  der  Lungengeschwulste,  Zeit.  f.  klin.  Med.,  1899,  xxxvii, 
435. 


442  DISEASES  OF  THE  LUNGS 

particles,  Hellendahl  recommends  filling  the  instrument  with  normal 
salt  solution  which  may  then  be  shaken  to  dislodge  the  smallest 
fragments.  The  contents  art'  then  expelled  and  carefully  examined. 
Or  the  syringe  may  be  partially  filled  with  normal  salt  solution  before 
the  puncture/  and  small  particles  prevented  from  clinging  to  the 
walls  of  the  instrument.  The  material  thus  obtained  may  be  hardened, 
cut,  and  stained.  The  method,  undertaken  solely  for  the  purpose 
of  diagnosis,  cannot  be  recommended.  Puncture  of  a  lung,  the  site 
of  new  growth  which  has  undergone  ulceration,  is  not  without  danger. 
Instrumental  injury  of  vascular  tissue  composing  the  new  growth, 
or  of  vessels  lining  the  walls  or  traversing  the  lumen  of  cavities  may 
be  the  source  of  fatal  hemorrhage.  Frankel1  refers  to  an  unfortunate 
experience  of  this  sort.  When  an  exploratory  puncture  has  been  made, 
however,  for  the  purpose  of  evacuating  pleural  fluid,  the  oppor- 
tunity of  examining  any  particles  obtained  during  the  procedure 
should  not  be  lost. »  Although  the  presence  of  malignant  disease  may 
be  established  in  this  way,  it  may  always  be  a  question  wdiether  the 
disease  is  primarily  pulmonary  or  pleural.  Both  cancer  and  sarcoma 
may  take  their  origin  from  the  pleura  as  well  as  the  lung. 

Examination  of  pleural  fluid  obtained  by  puncture  may  suggest 
the  diagnosis.  Involvement  of  the  pleura  in  the  new  growth  is  likely 
to  give  rise  to  hemorrhagic  fluid  of  a  type  corresponding  to  the  transu- 
dates. The  specific  gravity  is  likely  to  be  1018  or  under.  Desquamated 
endothelial  cells  from  the  free  surface  of  the  pleura  may  predominate 
in  the  sediment.  Atypical  cells,  in  few  or  many  of  which  mitoses  are 
observed,  may  afford  important  evidence.  An  abundance  of  spindle 
cells  may  establish  the  diagnosis. 

Some  evidence  of  the  intrathoracic  conditions  may  be  obtained 
during  the  puncture.  The  operator  may  note  a  sense  of  resistance  as 
if  the  instrument  were  penetrating  dense  pleural  or  pulmonary  tissue. 
It  may  be  difficult  or  impossible  to  decide  between  pleural  or  pulmo- 
nary resistance,  but  the  appearance  of  fluid  only  after  deeper  insertion 
through  dense  tissue  suggests  pleural,  while  a  successful  result  only 
after  partial  withdrawal  suggests  pulmonary  involvement.  Unex- 
pected, persistent  dyspnea  and  oppression,  dulness,  and  diminished 
or  absent  breathing  after  evacuation  of  pleural  fluid  may  also  be 
suggestive. 

Bronchoscopy. — The  successful  bronchoscopic  demonstration  of 
a  carcinoma  is  reported  by  V.  Schrotter.2  Several  examinations  were 
made.  A  flat,  yellowish  prominence  was  seen  on  the  anterior  wall 
of  the  right  primary  bronchus  (see  Fig.  75)  at  the  first  examination. 
During  the  course  of  about  four  months  the  tumor  increased  in  size 
until  it  almost  filled  the  bronchial  lumen,  leaving  only  a  small  slit 
posteriorly.  Ulceration  was  not  observed.  Microscopic  examination 
of  fragments  of  the  tumor  obtained  during  the  procedure  showed 

1  Spez.  Path.  u.  Ther.  d.  Lungenkrankheiten,  1904,  p.  953. 

2  Zeit.  f.  klin.  Med.,  1907,  vol.  lxii. 


TUMORS  OF  THE  BRONCHI  AND  LUNG 


443 


flat-celled  carcinoma.  At  autopsy  a  cancer  of  the  right  primary 
bronchus  with  carcinomatous  invasion  of  the  right  upper  lobe  was 
found.  Bronchoscopy  should  not  be  performed  by  other  than  experi- 
enced hands  and  is  even  then  not  without  danger.  The  possibility  of 
aortic  aneurysm  must  first  be  excluded. 

Fig.  75 


Bronchoscopic  demonstration  of  carcinoma  of  right  primary  bronchus.     (Schrotter.) 

Fig.  76 


Appearance  at  autopsy  of  carcinoma,  seen  by  bronchoscopy,  as  shown  in  Fig.  75. 
Partial  occlusion  of  right  primary  bronchus  by  tumor  arising  from  point  of  origin  of 
bronchus  to  the  right  upper  lobe.     (Schrotter.) 


Of  pulmonary  conditions,  primary  malignant  disease  is  most  likely 
to  be  confused  with  tuberculosis.  Cough,  pain,  dyspnea,  bloody 
sputum,  and  a  rapidly  downward  course  may  be  present  in  both 
affections.  In  typical  and  uncomplicated  cases,  however,  certain 
differences  may  be  noted.  A  family  history  of  tuberculosis  or  oppor- 
tunity for  contagion,  hemoptysis  or  pleurisy  as  an  initial  symptom, 
cough  with  abundant  purulent  sputum,  relatively  slight  dyspnea, 
without  thoracic  oppression,  early  and  persistent  fever  of  an  inter- 
mittent type,  night  sweats,  involvement  of  one  or  both  apices,  with 


444  DISEASES  OF  THE  LUNGS 

rales,  dulness,  bronchial  breathing,  increase  of  voice,  whisper  and 
tactile  fremitus,  certain  or  probable  evidence  of  previous  tuberculosis 
lesions  elsewhere  than  in  the  lung,  and  a  reaction  to  tuberculin  are  in 
favor  of  tuberculosis.  With  tumor,  on  the  contrary,  bloody  sputum 
is  more  likely  to  appear  late  than  early,  and  to  be  preceded  by  more 
severe  and  more  rapidly  progressive  dyspnea.  Intrathoracic  oppres- 
sion, cough,  scanty,  mucopurulent  rather  than  abundant  and  purulent 
sputum,  stridor,  absence  or  late  appearance  of  fever,  night  sweats 
only  in  rare  instances,  and  a  tendency  to  spare  the  apices  are  found  with 
tumor.  Over  the  involved  region  dulness  only  is  common  to  both 
tumor  and  tuberculosis.  With  tumor  the  affected  region  may  be  Hat 
and  resistant,  with  diminished  or  absent  breathing,  voice,  whisper 
and  tactile  fremitus,  without  rales.  Enlargement  of  accessible  lymph 
glands  and  the  signs  of  mediastinal  pressure  are  in  favor  of  tumor. 
Repeated  negative  search  for  tubercle  bacilli  in  the  expectoration  is 
of  some  moment  in  excluding  tuberculosis.  The  finding  of  tubercle 
bacilli  or  tumor  fragments  will  definitely  settle  the  diagnosis.  Tumor 
and  tuberculosis  at  times  coexist,  and  to  prove  the  presence  of  the 
one  does  not  necessarily  exclude  the  other. 

Degenerative  changes  in  the  tumor  with  cavity  formation,  stagna- 
tion of  secretion  in  parts  beyond  an  obstructed  bronchus,  bacterial 
infection  resulting  in  abscess,  gangrene,  bronchiectasis  and  interstitial 
pneumonia  may  so  obscure  the  presence  of  malignant  disease  as  to 
make  its  detection  difficult  or  impossible.  Echinococcus  cyst  may 
also  simulate  malignant  tumor. 

In  the  presence  of  a  mediastinal  growth  it  may  be  difficult  to  decide 
whether  this  has  arisen  by  metastasis  into  the  glands  from  a  primary 
tumor  of  the  lung  or  is  itself  primary  with  or  without  secondary  pul- 
monary involvement.  Primary  and  independent  mediastinal  tumors 
are  usually  sarcomata,  originating  in  the  mediastinal  connective  tissue 
or  lymph  glands,  the  peribronchial  lymph  glands  or  the  thymus.  They 
tend  to  form  more  rapidly  developing  and  extensive  growths  than  the 
secondary  cancerous  or  sarcomatous  deposits  in  this  region.  A  wider 
area  of  dulness  of  an  irregular  contour  may  therefore  be  expected. 
The  progress  of  the  affection  is  likely  to  be  different,  the  first  signs 
of  disturbance  being  referable  rather  to  the  mediastinum  than  the 
lung.  With  pulmonary  tumors,  on  the  contrary,  the  onset  is  likely 
to  be  with  dyspnea,  cough,  bloody  sputum,  pain  from  pleural  involve- 
ment, and  with  signs  of  pulmonary  or  pleural  invasion  earlier  in  the 
course  of  the  disease.  Radiographs  may  show  more  extensive  pul- 
monary involvement  than  can  be  determined  by  physical  examina- 
tion alone. 

The  same  difficulty  of  deciding  the  point  of  origin  obtains  between 
pulmonary  and  pleural  new  growths.  Early  metastasis  to  the  pleura 
from  the  lung  may  present  the  clinical  picture  of  a  primary  pleural 
disease.  It  may  in  general  be  said  of  primary  pleural  tumors,  how- 
ever, that  dyspnea  and  cough  are  not  usually  striking  features   at 


TUMORS  OF  THE  BRONCHI  AND  LUNG  445 

first;  bloody  sputum  is  less  often  present,  and  then  later  in  the  disease, 
while  the  features  of  onset  are  like  those  with  pleuritis.  Pain  is  usually 
a  prominent  symptom.  An  accumulation  of  pleural  fluid  is  almost 
constant. 

Aortic  aneurysm  may  simulate  secondary  as  well  as  primary  medias- 
tinal malignant  disease.  Venous  dilatation  is  more  common  and  more 
marked  with  tumor.  Metastases  in  accessible  regions  may  be  found. 
The  site  of  the  process,  more  uniform  outline  to  the  dulness,  stronger 
systolic  pulsation,  thrill,  murmurs,  fluoroscopic  and  radiographic 
examination  may  make  the  diagnosis  of  aneurysm  possible. 

Prognosis. — This  is  unfavorable.  The  duration  from  onset  to  fatal 
termination  is  variable,  but  is  usually  under  one  year,  over  two  years 
only  in  rare  instances.  In  Hellendahl's  case  the  duration  was  six 
years. 

Treatment. — This  is  unsatisfactory.  For  the  present,  palliative 
measures  alone  can  be  considered.  Heat  or  cold  may  be  applied 
locally  for  the  pain.  Fixation  may  also  be  tried.  Bromides  may  be 
of  service.  Resort  must  usually  be  made  sooner  or  later  to  opium 
or  its  derivatives  for  the  relief  of  a  distressing  and  ineffective  cough, 
pain  or  dyspnea.  The  removal  of  pleural  fluid  may  temporarily 
relieve  the  symptoms.     Repeated  withdrawal  may  be  necessary. 

Surgical  measures  for  malignant  disease  of  the  lung  have  been 
undertaken  only  in  rare  instances.  In  the  present  state  of  our  knowl- 
edge, primary  tumors  are  not  detected  at  a  sufficiently  early  stage  to 
offer  the  hope  of  cure.  The  uncommon  finding  at  autopsy  of  an  iso- 
lated small  primary  tumor,  without  metastases,  as  in  the  Massachu- 
setts General  Hospital  case  previously  mentioned,  indicates  that  com- 
plete and  successful  operative  removal  is  possible.  In  Haidenhein's1 
case  a  carcinomatous  nodule  the  size  of  a  hazel-nut  was  unexpectedly 
found  in  the  wall  of  a  bronchiectatic  cavity,  an  extensive  pulmonary 
resection  having  been  performed  for  bronchiectasis.  Surgical  inter- 
ference has  been  occasionally  attempted  for  secondary  malignant 
disease  of  the  lung.  The  cases  comprise  for  the  most  part  sarcomata 
or  chondromata  secondary  to  growths  in  the  thoracic  wall.  Tschekan2 
has  collected  12  cases,  including  one  of  his  own;  6  patients  died  witjiin 
the  first  24  hours  of  pneumothorax  or  collapse;  6  recovered  from 
the  operation.  In  the  latter  group,  Kronlein's  case  is  noteworthy. 
A  secondary  sarcoma  of  the  lung,  the  size  of  a  nut,  was  excised  from 
the  lung  of  a  girl,  aged  eighteen  years.  The  tumor  twice  reappeared 
in  the  scar  and  was  operated,  the  patient  dying,  however,  of  general- 
ization of  the  tumor  seven  years  after  the  first  operation.  Excision 
of  the  middle  and  lower  lobes  for  sarcoma  has  been  unsuccessfully 
performed  by  Helferich.3 

Little  can  be  expected  of  z-ray  treatment  of  deep-seated  malig- 

1  Centralbl.  f.  Chir.,  1901,  Kongressberichte,  p.  65. 

2  Allg.  med.  Central-Zeit.,  21  Mai,  1904,  p.  374. 

3  Deut.  Congress  f.  Chir.,  1898. 


1  ii;  DISEASES  OF  THE  LUNGS 

nant   disease.      Krukenberg1  noted   temporary   improvement  of  the 

pulmonary  metastases  in  a  patient  with  fibrosarcoma  under  .r-ray 
treatment. 

Secondary  Malignant  Disease  of  the  Lung.— This  is  much  more 
common.  Its' greater  frequency  may  he  judged  by  Reinhard's2  figures. 
Among  545  cancers'5  in  various  regions  the  lungs  were  secondarily 
involved  in  74,  while  in  only  5  cases  was  the  disease  primary  in  the 
lung. 

Of  178  cases  of  cancer  coming  to  autopsy  at  the  Massachusetts 
General  Hospital  the  lungs  were  secondarily  invaded  in  22  (12  per 
cent.)  Pulmonary  invasion  may  take  place  by  infiltration  from 
contiguity,  by  metastasis  through  lymph  or  bloodvessels,  and  probably 
also  by  inhalation  when  a  primary  growth  communicates  with  the 
respiratory  tract  above.  Secondary  deposits  in  the  lung  may  thus 
occur  from  primary  malignant  disease  in  nearby  or  remote  parts  of 
the  body,  but  are  more  likely  to  arise  in  connection  with  a  primary 
growth  in  neighboring  organs,  as  from  the  stomach  in  7  and  the  breast 
in  4  instances  in  this  series.  They  may,  however,  complicate  a  malig- 
nant growth  anywhere.  The  extent  of  the  pulmonary  involvement 
is  very  variable.  There  may  be  single  or  multiple  nodular  growths 
of  small  or  large  size.  Diffuse  invasion  is  less  common.  In  rare 
instances,  local  or  general  cancerous  lymphangitis  (miliary  carcino- 
sis) occurs.  Extension  by  continuity,  as  from  a  cancer  of  the  breast 
is  likely  to  give  rise  to  most  marked  pulmonary  involvement.  The 
disease  may  then  remain  unilateral  and  localized.  The  pleura  is 
usually  extensively  involved  when  the  disease  spreads  through  it  to 
the  lung  from  abdominal,  mammary  or  mediastinal  growths.  A 
diffuse  cancerous  pleuritis,  with  or  without  the  accumulation  of  sero- 
fibrinous or  hemorrhagic  fluid,  is  likely  to  follow.  In  rare  instances, 
however,  the  pleura  itself  may  be  spared,  although  the  infection  has 
apparently  passed  through  it  on  its  way  to  the  lung.  It  is  uncommon 
for  the  lungs  to  be  the  only  site  of  secondary  deposits.  The  histo- 
logic type  of  the  secondary  growth  is  usually  the  same  as  that  of  the 
primary  tumor. 

In  their  clinical  aspect  secondary  cancers  of  the  lung  present  a 
variable  picture.  The  pulmonary  process  is  not  infrequently  latent, 
and  is  first  discovered  at  the  postmortem  examination.  In  other 
instances  it  may  dominate  the  scene  and  obscure  symptoms  referable 
to  a  primary  growth  in  a  nearby  organ.  The  symptoms  and  physical 
signs  do  not  differ  from  those  in  primary  cancer  of  the  lung. 

Sarcoma  is  in  general  less  common  than  carcinoma,  and  thus  second- 
ary pulmonary  sarcoma  is  less  frequently  observed  than  secondary 
cancer.  Secondary  invasion  of  the  lung,  however,  is  relatively  more 
common  with  sarcoma  than  with  cancer.     Of  42  cases  coming  to 

1  Fortschr.  a.  d.  Gebiete  d.  Rdntgenstr.,  1912-13,  exci,  383. 

2  Arch.  f.  Hcilkunde,  1878,  vol.  xix. 

3  Carcinoma  and  sarcoma  were  not  differentiated. 


TUMORS  OF  THE  BRONCHI  AND  LUNG  447 

autopsy  at  the  Massachusetts  General  Hospital  with  sarcoma  in 
various  regions,  the  lungs  were  secondarily  invaded  in  15  (35  per  cent.) 
The  lungs  are  a  common,  and  may  be  the  only,  site  of  secondary 
deposits  from  sarcoma  in  various  parts  of  the  body.  In  general  the 
pathologic  and  clinical  features  do  not  differ  from  those  in  secondary 
cancer.  At  times  the  histologic  type  of  the  original  growth  is  not 
reproduced,  and  thus  a  pulmonary  metastasis  from  an  osteosarcoma 
or  chondrosarcoma  developing  elsewhere  may  contain  neither  bone 
nor  cartilage.  Pulmonary  deposits  from  a  melanotic  sarcoma  may 
likewise  fail  to  show  pigmentation. 


CHAPTER  XXVII. 
LUNG  HERNIA   (PNEUMONOCELE) 

By  this  is  understood  the  protrusion  of  a  part  of  the  lung  through 
a  defect  in  the  chest  wall,  the  thoracic  defect  being  covered  by  skin. 
Diaphragmatic  hernia  is  not  considered  here  but  is  discussed  in  the 
section  on  Pneumothorax. 

The  first  observation  on  lung  hernia  is  ascribed  to  Roland  (1499). 
Contributions  to  the  subject  have  been  made,  among  others,  by 
Morelle-Lavelle,1  Auer,2  who  collected  51  cases,  and  by  Urbach,3 
who  added  33  cases.  A  few  additional  instances  have  since  been 
reported. 

Two  groups  may  be  recognized:  Congenital  hernia  develops  usually 
within  a  short  interval  after  birth  in  infants  born  with  defects  in  the 
chest  wall.  Owing  to  the  collapsed  and  airless  condition  of  the  lung 
before  birth,  hernia  does  not  occur  in  utero,  but  first  appears  after 
the  lung  becomes  air-holding,  and  probably  in  consequence  of  crying 
or  coughing.  In  Polya's4  case,  development  of  a  hernia  due  to  con- 
genital defect  of  the  thorax  was  delayed  until  adult  life.  Acquired 
hernia  may  follow  trauma,  when  the  thoracic  wall  is  torn,  crushed, 
or  perforated  without  a  break  in  the  continuity  of  the  overlying  skin 
in  consequence  of  the  injury.  The  defect  in  the  wall  may  involve 
the  intercostal  muscles  alone  or  the  bony  structures  as  well.  The 
hernia  may  occur  at  once  or  develop  after  a  time  through  less  resistant 
scar  tissue  (consecutive  lung  hernia).  In  Trevisano's5  case  a  hernia 
occurred  at  the  site  of  repeated  punctures  of  the  chest  on  account 
of  pleurisy  with  effusion.  The  hernia  may  be  due  to  a  defect  from 
extension  of  suppuration  from  the  lung  or  pleura  to  the  chest  wall  or 
abscess  of  the  wall  itself  (such  as  caries  of  the  rib).  The  location  of 
hernia  due  to  trauma  or  pathologic  intrathoracic  or  thoracic  pro- 
cesses is  variable  and  depends  on  the  site  of  the  resulting  defect  in  the 
wall.  In  a  few  instances,  hernia  occurs  as  a  consequence  of  increased 
intrathoracic  pressure  in  connection  with  emphysema  and  chronic 
cough  or  severe  physical  exertion,  especially  heavy  lifting,  the  so- 
called  spontaneous  hernia.  The  intercostal  spaces  near  the  sternum 
and  the  supraclavicular  fossse  (between  the  scaleni  and  jthe  sterno- 
cleidomastoids) are  likely  to  be  the  site  of  the  rupture  in  this  form. 

1  Hernies  du  poumon.,  Mem.  de  la  soc.  de  Chir.,  1847. 

2  Beitrag  z.  Kenntniss  d.  Lengenbruche,  Inaug.  Diss.,  1892. 

3  Ueber  Lungenhernien,  Deut.  Zeit.  f.  Chir.,  1909,  cii,  89. 

4  Pester  med.-chir.  Presse,  1909,  No.  13;   quoted  from  Centralbl.  f.  Chir.,  1909,  p.  923. 

5  Gaz.  degli  osped.  e  stelle  cliniche,  1904,  No.  16. 


LUNG  HERNIA 


449 


One  instance  (No.  188,499)  of  lung  hernia  in  the  right  supraclavicular 
region  is  recorded  among  the  Massachusetts  General  Hospital  cases. 
Pain  may  be  felt  at  the  site  of  the  hernia  and  is  likely  to  be  increased 
with  long  breath  or  cough.  It  may  be  troublesome  enough  to  prevent 
severe  exertion  or  incapacitate  the  patient  from  work.  The  pain  is 
more  pronounced  in  the  early  period  after  the  development  of  the 
hernia  and  may  diminish  or  disappear  later.  Hemoptysis  has  been 
observed. 

Fig.  77 


Lung  hernia.      (GoLdflam.) 


The  hernia  forms  a  rounded  tumor  covered  by  skin  or  scar  tissue 
and  varies  in  size  from  that  of  a  hazel-nut  to  two  fists.  Increase 
in  size  may  be  observed  during  forced  expiration,  cough,  or  bending 
forward,  diminution  or  disappearance  in  size  during  quiet  respiration, 
during  inspiration  or  on  standing  erect.  It  is  soft,  elastic  and  reduc- 
ible, unless  held  by  adhesions.  Crepitation  may  be  felt  on  compres- 
sion and  during  reduction.  A  more  or  less  circular,  oval,  slit-like 
or  irregular  orifice  may  be  felt  in  the  chest  wall  after  reduction.  The 
tumor  is  usually  resonant  or  tympanitic  on  percussion.  Vesicular 
breathing  and  expiratory  crepitation  may  be  noted  on  auscultation. 
The  voice  sounds  and  the  tactile  fremitus  are  increased.  The  hernia 
may  be  constant  or  intermittent  and  present  only  during  forced  expira- 
tion, cough,  or  exertion.  Bilateral  hernias  have  been  observed  in  rare 
instances.  Strangulation  of  the  hernia  took  place  in  Wightman's1 
case. 

1  British  Med.  Jour.,  February,  1898,  p.  365. 
29 


i:,o 


DISEASES  OF  THE  LUNGS 


Lung  hernia  must  be  differentiated  from  tumors  of  the  thoracic 
wall,  perforating  lung  abscess,  empyema  necessitatis,  and  aneurysm. 
In  one  instance  which  came  under  my  observation  a  pyopneumothorax 
which  perforated  the  chest  wall  in  the  third  left  interspace  was  at 
first  mistaken  for  lung  hernia. 


Fig 


Lung  hernia.      (Volpius.) 


The  hernia  may  remain  stationary,  increase  in  size  from  gradual 
enlargement  of  the  orifice,  or  diminish  and  finally  disappear.  The 
condition  is  rather  troublesome  than  dangerous. 

Any  underlying  condition  giving  rise  to  cough  should  be  appro- 
priately treated.  Severe  physical  exertion  and  straining  at  stool  are 
to  be  avoided.  The  hernia  should,  if  possible,  be  reduced,  and  recur- 
rence prevented  by  the  application  of  a  suitable  truss.  Osteoplastic 
closure  of  a  large  thoracic  hernial  orifice  was  attempted  by  Vulpius1 
with  partial  success. 

1  Berl.  klin.  Woch.,  1900,  No.  50. 


CHAPTER  XXVIII. 
PULMONARY  ARTERIOSCLEROSIS. 

The  pulmonary  artery  and  its  branches  may  show  arteriosclerotic 
changes  similar  to  those  observed  in  the  systemic  arteries.  A  widely 
distributed  and  severe  grade  of  sclerosis  is  occasionally  found. 
Crudeli1  and  Wolfram2  have  each  described  an  instance  of  aneurysmal 
dilatation  of  the  pulmonary  artery  in  connection  with  arteriosclerotic 
changes  in  the  vessel.  Sclerotic  changes  without  the  formation  of 
aneurysm  have  been  observed  by  Klob,3  Romberg,4  Aust,5  Bruning,6 
Torhorst,7  Fischer8  and  others.  Fischer  systematically  investigated 
a  large  amount  of  pathologic  material  and  found  sclerotic  changes 
in  the  pulmonary  arteries  in  100  out  of  700  autopsies.  Coincident 
arteriosclerosis  is  usually  present  in  the  aorta  and  other  systemic- 
arteries,  but  in  some  instances  the  pulmonary  artery  and  its  branches 
are  predominantly  or  apparently  exclusively  involved. 

A  secondary  and  a  primary  form  have  been  described.  In  most 
instances  such  other  lesions  as  emphysema,  mitral  disease,  especially 
stenosis,  extensive  pleural  adhesions  or  chronic  interstitial  pneu- 
monia have  suggested  that  increase  of  pressure  in  the  pulmonary 
circuit  and  consequent  embarrassment  of  the  circulation  may  be 
responsible.  Syphilis  may  also  be  a  factor.  In  two  instances  (Autop- 
sies 2572  and  2788)  among  the  Massachusetts  General  Hospital  cases 
a  marked  degree  of  arteriosclerosis  was  found  in  the  pulmonary  artery 
and  its  branches.  In  rare  instances,  as  in  the  cases  reported  by 
Monckeberg9  and  Sanders,10  the  pulmonary  arterial  changes  are 
unassociated  with  significant  lesions  in  the  lungs  or  other  parts  of 
the  circulatory  apparatus,  to  which  they  could  be  regarded  as  second- 
ary. Hypertrophy  and  dilatation  of  the  right  side  of  the  heart  are 
usually  present  in  both  groups.  The  cause  is  uncertain  in  the  primary 
cases.  The  development  of  the  arterial  lesions  at  thirty- three  years 
of  age  in  Sander's  and  one  of  Monckeberg's  cases,  suggests  the  possi- 
bility of  a  congenital  alteration  in  the  vessel  wall. 

The  appearances  in  pulmonary  arteriosclerosis  are  in  general  simi- 
lar to  those  in  arteriosclerosis  of  the  aorta  and  its  branches.    There 

1  Riv.  clin.,  vii,  2,  p.  37. 

2  Gaz.  lekarska,  1883,  Nos.  24  and  25.     See  Virchow-Hirsch's  Jahresber.,  1883,  ii,  162. 

3  Wien.  Wochenbl.,  1865,  xxi,  45. 

4  Deut.  Arch.  f.  klin.  Med.,  18,91,  xlviii,  197. 

6  Munch,  med.  Woch.,  1892,  p.  689.  6  Ziegler's  Beitrage,  Bd.  xxx,  p.  457. 

7  Ibid.,  Bd.  xxxvi. 

8  Deut.  Arch.  f.  klin.  Med.,  1909,  lcvii,  230. 

9  Deut.  mcd.  Woch.,  August  1,  1907.  10  Arch.  Int.  Med.,  1909,  iii,  257. 


452  DISEASES  OF  THE  LUNGS 

may  be  yellowish  or  yellowish-white  flat  projections  of  variable  size 
in  the  pulmonary  artery  and  usually  most  often  just  above  the  pul- 
monary valves.  Similar  areas  may  be  found  in  the  primary  branches 
and  their  medium  and  smaller  divisions,  at  times  in  greater  abund- 
ance about  tlie  orifices  of  the  branches.  This  represents  the  nodular 
form.  Diffuse  sclerotic  changes  may  also  be  observed.  The  arteries 
may  be  dilated  as  far  as  their  finest  divisions.  Stiffness  of  the  vessels 
may  be  noted.  Softening  with  the  formation  of  atheromatous  ulcers 
was  not  observed  in  any  of  Fischer's  cases.  Microscopic  examination 
shows  thickening  of  the  intima  from  increase  of  connective  tissue. 
Fatty  degeneration  and  at  times  calcification  may  be  noted.  Less 
marked  degeneration  of  the  media  in  the  form  of  isolated  fatty  and 
hyaline  changes  may  also  be  present. 

The  clinical  features  are  those  of  cardiac  failure,  with  dyspnea  and 
other  evidence  of  stasis  in  the  venous  system.  In  Romberg's  case 
a  congenital  cardiac  lesion  was  suspected  on  account  of  the  extreme 
cyanosis.  Examination  of  the  heart  may  show  enlargement  to  the 
left  in  consequence  of  hypertrophy  and  dilatation  of  the  right  ventri- 
cle. An  increase  in  size  to  the  right  of  the  sternum  may  be  demon- 
strable if  the  right  auricle  is  hypertrophied  or  dilated.  In  some  cases, 
dulness  has  been  noted  in  the  left  second  interchondral  space  and  may 
be  ascribed  to  dilatation  of  the  pulmonary  artery.  Various  murmurs 
may  be  heard.  A  systolic,  rough  murmur  confined  to  the  second  left 
interchondral  space  may  be  due  to  roughening  of  the  pulmonary 
artery.  A  diastolic,  blowing  murmur  in  the  same  region  and  trans- 
mitted downward  along  the  left  edge  of  the  sternum,  without  other 
signs  suggestive  of  aortic  regurgitation,  may  be  due  to  insufficiency 
of  the  pulmonary  valves.  Accentuation  of  the  second  sound  in  the 
second  left  interchondral  space  may  also  be  present.  It  is  possible  that 
examination  with  the  .r-rays  may  afford  evidence  of  dilatation  and 
calcification  of  the  pulmonary  artery.  The  signs  are  difficult  to  inter- 
pret and  the  diagnosis  has  as  yet  not  been  made  during  life  and 
confirmed  at  postmortem  examination. 


SECTION  III. 
DISEASES  OF  THE  PLEURA. 


CHAPTER  XXIX. 
PLEURITIS.1 

Historical. — The  term  "pleuritis"  was  in  use  previous  to  the  time  of 
Hippocrates,  but  designated  any  febrile  disease  accompanied  by  pain 
in  the  side,  and  thus  included  disease  of  neighboring  organs  as  well 
as  the  pleura.  Hippocrates  and  Galen  separated  peripneumonia 
from  pleuritis,  which  was  regarded  as  an  affection  of  the  costal  pleura 
alone.  Boerhaave  was  the  first  to  establish  the  site  of  pleurisy  exclu- 
sively in  the  pleura,  a  view  which  Van  Swieten  shared,  while  Syden- 
ham, Haller,  and  Morgagni  believed  that  both  lung  and  pleura  were 
often,  if  not  always,  involved  together.  Pinel  was  the  first  to  class 
pleuritis  definitely  as  an  inflammation  of  the  serous  membranes  and 
to  regard  it  as  an  independent  disease,  from  the  anatomic  lesions. 
Laennec's  masterly  account  of  pleuritis  and  its  recognition  laid  the 
foundation  for  our  present  knowledge,  and  since  his  time  little  advance 
has  been  made  in  diagnosis  by  physical  signs.  More  accurate  ana- 
tomic and  pathologic  knowledge  has  led  to  a  better  understanding  of 
the  relation  between  diseases  of  the  lung  and  the  pleura,  of  the  value 
of  thoracentesis,  of  the  importance  of  tuberculosis  in  pleurisy,  and  of 
the  diagnostic  value  of  various  forms  of  cells  in  pleural  fluids. 

Thoracentesis. — The  evacuation  of  pleural  fluid  by  operation  dates 
back  to  a  remote  and  uncertain  period.  The  legend  runs,  as  Cicero 
and  Pliny  relate,  that  the  suggestion  of  operation  had  its  origin  in 
the  wounding  of  Pheraeus  who,  told  by  his  physicians  that  he  had  an 
incurable  ulcer  on  the  lungs,  exposed  himself  in  battle  that  he  might 
be  slain,  but  the  enemy's  weapon  pierced  his  side,  allowing  the  pus  to 
escape,  and  he  recovered. 

1  The  statistical  data  on  pleuritis  are  from  three  sources:  (1)  The  Massachusetts 
General  Hospital  (M.  G.  H.),  Boston;  (2)  the  Presbyterian,  and  (3)  Roosevelt  Hospitals, 
New  York.  I  am  greatly  indebted  to  W.  B.  James,  of  New  York,  for  his  kindness  in 
placing  many  valuable  data  on  diseases  of  the  pleura  at  my  disposal.  The  M.  G.  H.  data 
were  in  great  part  gathered  by  C.  L.  Overlander.  The  hospital  records  are  rich  in  data  on 
the  cytology  of  pleural  fluids,  much  of  the  work  on  which  was  done  by  P.  Musgrave. 


454  DISEASES  OF   THE  PLEURA 

Galen  states  that  the  life  of  Cinesias  was  saved  by  Euryphon,  of 

('nidus,  who  opened  the  chest  with  the  actual  cautery.  The  operation 
was  frequently  performed  in  the  time  of  Hippocrates.  The  diagnosis 
was  made  from  observation  of  the  breathing,  fever,  pain  and  cough, 
succussion  sounds,  the  position  of  the  patient,  and  swelling  of  the 
side.  Evacuation  was  accomplished  by  the  actual  cautery,  the  knife, 
and  perforation  of  a  rib.  The  operator  is  cautioned  to  prepare  for 
operation  by  washing  the  patient  with  warm  water.  Celsus  and  Galen 
employed  the  operation,  but  it  was  regarded  as  dangerous  and  was 
largely  given  tip  among  the  Greeks  and  Romans.  In  the  sixteenth 
century  the  operation  was  again  recommended,  among  others,  by 
Ambroise  Pare,  but  was  seldom  done  except  in  extreme  cases.  It  was 
often  practised  in  the  seventeenth  and  eighteenth  centuries,  but  had 
many  opponents,  and  was  usually  unsuccessful.  Dupuytren  had  only 
4  recoveries  in  50  cases,  and  himself  died  of  empyema,  saying  of  him- 
self that  he  would  rather  die  by  the  hand  of  God  than  of  man.  Druin, 
about  the  year  1665,  proposed  the  use  of  the  trocar  as  a  substitute 
for  the  actual  cautery  in  opening  the  chest.  Aspiration  was  employed 
by  Scultetus  in  1669.  An  incision  was  made  with  the  knife,  and  by 
puncture  with  the  sharp  cannula.  Suction  was  applied  by  the  mouth, 
by  cups,  and  by  syringes. 

The  great  improvement  in  the  diagnosis  of  thoracic  disease  follow- 
ing Laennec's  publications  did  not  exert  an  immediate  influence  on 
the  question  of  thoracentesis,  but  finally  overcame  previously  existing 
indecision.  Laennec,  himself,  was  not  an  earnest  advocate  of  opera- 
tion, and  states  that  he  never  obtained  any  lasting  success  by  its  use. 
He  recommended  operation  in  acute  pleurisy  with  fluid  accumulation, 
when  at  the  end  of  some  days  there  is  danger  of  suffocation,  and  in 
chronic  cases,  where  other  means  have  failed.  He  advised  puncture 
with  the  trocar  when,  owing  to  weakness,  the  total  evacuation  of  the 
fluid  may  cause  dangerous  syncope  or  as  a  means  of  alleviation  in 
hopeless  cases. 

Among  others  in  Germany,  Becker  (1834),  Schuh  and  Skoda  (1841), 
and  Wintrich  (1854);  in  France,  Trousseau  (1843),  Marotte  (1854), 
and  Sedillot  (1855);  and  in  England  (1844),  Hughes  and  Cock,  Roe 
and  Thompson,  advocated  thoracentesis.  In  America  at  this  time 
the  general  opinion  was  against  the  procedure.  As  Bowditch  wrote 
in  1851,  the  operation  "is  strongly  advocated  by  a  few  and  as  strongly- 
opposed  by  others,  and  looked  upon  with  indifference  by  the  great 
mass  of  European  physicians." 

In  1849  or  1850  H.  I.  Bowditch,1  who  had  long  been  impressed 
with  the  necessity  of  operation  for  pleural  fluids,  was  confirmed  in 
this  opinion  by  the  paper  of  Hughes  and  Cock.  In  1850,  he  saw  a  case 
which,  in  his  opinion,  demanded  tapping,  and  called  Morrill  Wyman 
in  consultation.     The  operation  was  done  by  Wyman,  who  used  an 

1  Amer.  Jour.  Med.  Sci.,  1852. 


PLEURITIS  455 

instrument  devised  by  him,  consisting  of  an  exploring  trocar  to  which 
was  attached  a  strong  suction  pump.  From  this  time  Bowditch 
became  an  earnest  advocate  of  aspiration,  and  by  his  publications 
did  more  than  any  other  to  introduce  the  method  into  practice  in 
America  and  Germany.  His  conclusions  as  to  the  indications  for 
operation  are  of  historic  interest,  and  very  nearly  represent  the 
opinion  of  the  present  day,  viz.,  to  operate  in  acute  or  chronic  cases 
where  the  chest  is  full  and  distended  with  fluid,  even  without  dysp- 
nea; where  there  is  alarming  or  paroxysmal  dyspnea,  even  if  the 
chest  be  only  partially  filled  with  fluid;  in  all  acute  cases  where  the 
remedies  employed  do  not  produce  ready  absorption,  and,  "further- 
more, as  it  may  be  of  service  in  relieving  dyspnea  and  helping  on  the 
more  rapid  cure,  it  may,  therefore,  become  a  question  whether  even 
a  small  quantity  of  fluid  should  not  be  removed  within  a  week  after 
the  first  attack  of  acute  pleurisy." 

The  apparatus  for  aspiration  has  undergone  certain  important 
modifications.  In  1858,  Thompson1  described  a  lateral  outlet  from 
the  body  of  the  cannula.  This  was  modified  by  Fraenzel2  in  1874  by 
adding  a  stopcock  in  the  lateral  outlet  and  a  device  for  preventing  the 
entrance  of  air  into  the  body  of  the  cannula  when  the  stylet  is  with- 
drawn. In  1869,  Dieulafoy  devised  an  aspirator  consisting  of  a  fine 
needle  connected  by  a  rubber  tube  to  an  apparatus  in  which  the  air 
can  be  exhausted.  In  1872,  Potain  and  Castiaux,  in  Paris,  and  von 
Rasmussen,  in  Copenhagen,  suggested  the  bottle  aspirator  in  which 
negative  pressure  is  maintained  by  an  air  pump.  Dieulafoy's  rack 
aspirator  and  Potain's  bottle  method  are  still  much  in  use.  By  the 
use  of  these  instruments  the  entrance  of  air  into  the  pleural  sac  during 
aspiration  is  prevented,  thus  obviating  the  danger  of  artificial  pneumo- 
thorax and  possible  infection  of  the  pleura. 

Aspiration  in  both  serous  and  purulent  effusions  was  at  first  a  com- 
mon practice,  but  aspiration  is  now  generally  restricted  to  other  than 
purulent  fluids  and  free  incision  is  used  for  empyema. 

Occurrence. — From  the  point  of  view  of  the  pathologist,  the  occur- 
rence of  pleuritis  is  very  frequent.  Including  simple  adhesions  with 
other  more  marked  changes  in  the  pleura,  pleuritis  was  found  in  160 
(74.4  per  cent.)  of  215  cases  at  autopsy  (M.  G.  H.).  Such  processes 
pass  unheeded  or  undiagnosed  in  the  great  majority  of  patients,  as  is 
shown  by  the  striking  disparity  between  autopsy  and  clinical  reports. 
Thus,  of  35,207  patients  admitted  to  the  medical  wards  of  the  Massa- 
chusetts General  Hospital  from  1897  to  1913  inclusive,  only  975  (2.7 
per  cent.)  are  recorded  as  suffering  from  pleuritis.  Fraley's3  figures 
for  the  Pennsylvania  Hospital  are  nearly  the  same,  505  (2.5  per 
cent.)  in  19,396  cases.  Gerhardt  reports  3.47  per  cent,  of  cases  with 
pleuritis  in  Wiirzburg  among  medical  patients  during  thirteen  years, 
and  0.9  per  cent,  in  eight  years  at  the  Charite  in  Berlin.     Uncom- 

1  Med.  Times  and  Gaz.,  1858,  p.  329.  2  Berl.  klin.  Woch.,  1S74,  vol.  xii. 

3  Amer.  Jour.  Med.  Sci.,  May,  1907. 


456  DISEASES  OF  THE  PLEURA 

plicated  inflammation  of  tin*  pleura  is  not  a  frequent  cause  of  death. 
Thus,  of  2,642, 555  deaths  recorded  in  the  United  States  Census  Report 
for  five  years  (1900  to  1904),  only  7420  (0.2  per  cent.)  are  assigned 
to  pleurisy. 

General  Etiology. — Age. — Pleuritis  has  been  described  in  the  new- 
born, but  is  relatively  uncommon  in  infants.  Wrany  (quoted  from 
Gerhardt)  noted  pleuritic  adhesions  in  infants  of  fifteen  days  and 
three  weeks.  Holt  states  that  the  youngest  case  in  which  he  has  found 
extensive  pleuritic  adhesions  is  in  an  infant  of  three  months.  Baron1 
found  evidence  of  pleuritis  in  159  of  403  autopsies  on  children.  Pleu- 
ritic effusions  in  children  are  more  often  purulent  and  metapneumonic 
in  origin,  while  in  adults  serous  and  tuberculous  pleuritis  is  more 
common. 

The  relation  of  age  differs  somewhat  between  clinical  and  mortality 
statistics.  Of  760  clinical  cases  (M.  G.  H.)2  of  different  forms  of 
pleuritis,  63  were  ten  and  under,  114  eleven  to  twenty,  255  twenty- 
one  to  thirty,  178  thirty-one  to  forty,  83  forty-one  to  fifty,  51  fifty-one 
to  sixty,  12  sixty-one  to  seventy,  while  4  were  seventy-one  to  eight}'. 
Thus,  about  one-third  of  the  cases  occurred  from  twenty-one  to  thirty 
and  more  than  one-half  from  twenty-one  to  forty.  In  mortality 
returns,  the  cases  are  much  more  evenly  distributed  through  the 
different  ages,  with  a  larger  proportion  at  the  extremes  of  life.  Of 
74203  cases  in  the  United  States  Census  Report  for  five  years  (1900  to 
1904)  certified  as  dying  from  pleuritis,  there  are  997  under  five  (302 
under  one),  425  from  five  to  fourteen,  755  from  fifteen  to  twenty-four, 
938  from  twenty-five  to  thirty-four,  974  from  thirty-five  to  forty-four, 
1897  from  forty-five  to  sixty-four,  and  1415  sixty-four  or  over.  These 
figures  suggest  that  pleuritis  is  less  common  but  more  fatal  at  the 
extremes  of  age. 

Sex. — In  general,  males  are  much  more  frequently  affected.  In  my 
series  of  1681  patients  with  fibrinous,  serofibrinous,  or  purulent  pleu- 
ritis, 1213  were  males,  468  females.  In  the  United  States  Census 
Report  (1900  to  1904)  there  were  4251  males,  3169  females.  There 
appears  to  be  no  striking  difference  in  the  relation  of  sex  at  the 
different  ages  or  in  the  different  forms  of  pleuritis,  males  in  general 
exceeding  females. 

Occupation. — The  relation  between  pleuritis  and  occupation  may 
be  considered  to  be  that  of  the  diseases  to  which  pleuritis  is  most 
often  secondary.  Thus,  occupations  predisposing  to  pulmonary 
tuberculosis  or  other  respiratory  infections  may  indirectly  lead  to 
pleuritis.  As  in  tuberculosis,  its  influence  is  largely  referable  to  poverty, 
poor  ventilation,  overcrowding,  an  inadequate  wage,  and,  perhaps  most 
important  of  all,  ignorance  in  the  disposal  of  infected  material.  Those 
occupations  in  which  there  is  the  greatest  amount  of  dust,  aiding 

1  Journ.  f.  Kinderkrankheiten,  vol.  i,  p.  20. 

2  Children  comprise  only  a  small  number  of  the  total  admissions. 

3  Age  unknown  in  19  cases. 


PLEURITIS  457 

in  the  distribution  of  expectorated  bacilli,  may  most  often  be  expected 
to  lead  to  tuberculous  pleuritis.  The  tabulation  of  occupation  and 
pleurisy  with  effusion  in  279  cases  (M.  G.  H.)  shows  that  dusty  employ- 
ment obtained  in  60  (21.5  per  cent.). 

Season. — Since  respiratory  infection  occurs  more  often  during  the 
colder  months  of  the  year,  and  because  of  the  frequent  association  of 
pulmonary  and  pleural  infection,  a  similar  relation  with  the  seasons 
may  be  expected  to  obtain  in  pulmonary  and  pleural  infection.  This 
has  been  shown  to  be  the  case.  It  is  confirmed  by  762  patients,  of 
whom  248  (32.5  per  cent.)  sought  the  hospital  clinic  during  March, 
April,  or  May,  the  greatest  number  of  cases  for  any  month  being  94 
in  March;  while  189  (24.8  per  cent.)  presented  themselves  in  June, 
July,  or  August,  178  (23.3  per  cent.)  in  December,  January,  or  Feb- 
ruary, and  147  (19.2  per  cent.)  in  September,  October,  or  November. 

Exposure. — With  the  growth  of  knowledge  concerning  the  role  of 
bacteria  in  the  disease,  exposure  has  come  to  be  regarded  as  of  little 
moment  as  a  principal  cause.  It  cannot,  however,  be  totally  disre- 
garded, but  must  be  looked  upon  rather  as  a  contributing  factor  in 
certain  cases.  It  is  probable  that  in  some  unexplained  way  it  favors 
the  development  of  organisms  already  present  in  the  respiratory  tract. 
Of  467  cases  of  fibrinous  and  serofibrinous  effusion  it  was  a  possible 
contributing  cause  in  34  (7.2  per  cent.). 

Bacterial  Etiology. — As  yet  it  is  impossible  to  separate  the  inflam- 
mations of  the  pleura  into  sharply  defined  groups  according  to  their 
bacterial  etiology,  with  a  characteristic  clinical  picture,  pathology, 
course,  and  termination.  Fibrinous,  serofibrinous,  or  purulent  pleu- 
ritis may  be  due  to  one  or  more  different  organisms  in  the  same  or  in 
different  cases.  The  number  of  organisms  concerned  is  comparatively 
small,  and  in  the  great  majority  of  cases  comprises  the  tubercle  bacillus, 
the  pneumococcus,  or  the  streptococcus.  Pleural  fluids,  from  the 
readiness  with  which  they  can  be  obtained  for  examination,  are  the 
most  promising  field  for  investigation,  but  fluids,  in  other  respects 
similar  so  far  as  our  present  methods  go,  may  show  different  bacteria. 

The  limited  number  of  different  organisms  concerned  is  probably 
due  to  the  relation  of  the  pleura  to  the  deeper  parts  of  the  respiratory 
tract,  where  mixed  infections  are  less  common.  The  tendency  of  the 
tubercle  bacillus  to  invade  the  subpleural  tissue  or  the  thoracic  glands 
in  close  relation  with  the  pleura  is  well  known,  and  explains  its  fre- 
quent invasion  of  the  pleura. 

Tubercle  Bacillus. — This  is  a  frequent  cause  of  pleuritis,  either  alone 
or  in  combination  with  other  organisms,  but  it  is  not  yet  possible  with 
any  degree  of  accuracy  to  state  in  what  proportion  of  cases  it  is  a 
factor  in  the  different  forms.  It  is  undoubtedly  one  of  the  most  com- 
mon but  not  the  only  cause  of  fibrous  adhesions  and  scars  so  commonly 
found  in  the  pleura  and  most  often  at  the  apices.  In  many  instances 
these  are  the  result  of  extension  of  inflammation  about  tuberculous 
foci,  evidence  for  which  is  afforded  by  the  presence  in  the  underlying 


t58  DISEASES  OF  THE  PLEURA 

pulmonary  tissue  of  caseous,  fibrocaseous,  or  calcified  areas.  When  not 
so  associated,  they  cannot  he  regarded  as  necessarily  tuberculous  in 

origin,  and  may  arise  from  preceding  inflammation  due  to  other  organ- 
isms. The  tubercle  bacillus  with  other  organisms  is  at  times  undoubt- 
edly a  cause  of  'fihrinous  pleuritis,  and  tubercles  may  be  found  in  such 
tissue.  The  failure  to  find  other  organisms  than  the  tubercle  bacillus 
in  purulent  pleural  exudates  does  not  establish  their  independent 
relation  with  the  latter,  for  other  organisms  may  have  been  present 
and  died  out. 

The  tubercle  bacillus  plays  a  most  important  part  in  serous  effusions, 
in  which  it  has  been  demonstrated  in  from  22  to  85  per  cent,  by  differ- 
ent observers  as  a  contributing  or  principal  cause.  At  present  we  have 
no  certain  means  of  excluding  it,  and  it  may  still  exist  even  with  nega- 
tive inoculation  experiments. 

Pneumococcus. — The  pneumococcus  may  be  a  cause  of  fibrinous, 
serofibrinous,  or  purulent  pleuritis.  It  is  a  common  factor  in  the 
fibrinous  form.  It  is  only  rarely  a  cause  of  clear  serous  effusions,  but 
is  more  common  in  turbid  exudates  and  is  frequent  in  purulent  effusions. 
It  is  common  in  the  primary  empyemas  of  children  and  in  all  effusions 
complicating  lobar  pneumonia. 

Streptococcus. — This  is  less  common  in  serofibrinous  exudates  than 
the  pneumococcus,  but  is  not  infrequently  present  in  empyema.  It 
is  common  in  suppurative  pleuritis  secondary  to  such  diseases  of  the 
lung,  as  lobar  pneumonia  and  bronchopneumonia,  abscess,  gangrene, 
bronchiectasis,  following  trauma  to  the  chest  wall  or  septic  processes 
in  more  remote  parts  of  the  body. 

Other  Organisms. — Staphylococcus  pyogenes  aureus  is,  perhaps,  the 
next  most  common  organism  found  in  pleural  exudates.  Streptococcus 
mucosus  capsulatus,  influenza  bacillus,  Friedlander's  bacillus,  diphtheria 
bacillus,  micrococcus  tetragenus,  bacillus  ramosus,  bacillus  pyocy- 
aneus,  and  bacillus  subtilis  have  been  occasionally  found,  either  alone 
or  in  combination,  and  at  times  associated  with  the  tubercle  bacillus, 
the  pneumococcus,  or  the  streptococcus  in  purulent  exudates.  The 
typhoid  bacillus  has  rarely  been  cultivated  from  pleural  fluids  of  a 
serofibrinous,  hemorrhagic,  or  purulent  character.  The  demonstra- 
tion of  an  organism  with  the  morphology,  staining  reaction,  and 
cultural  peculiarities  of  the  gonococcus  is  reported  by  Bordoni- 
Uffreduzzi.1    The  cultures  are  not  described. 

Classification. — It  is  impossible  at -present  to  classify  the  inflam- 
mations of  the  pleura  satisfactorily  according  to  their  etiology.  The 
most  convenient  and  practical  division  is  into  acute  and  chronic 
pleuritis,  each  of  which  may  be  primary  or  secondary,  and  accord- 
ing to  the  clinical  or  pathologic  findings,  fibrinous,  serofibrinous,  or 
purulent.  The  terms  "primary"  and  "secondary"  are  convenient 
for  the  description  of  clinical  cases,  but  are  somewhat  misleading  and 

1  Deutsch.  mod.  Woch.,  1894,  No.  22. 


ACUTE  FIBRINOUS  PLEURITIS  459 

need  a  word  of  explanation.  Pleuritis  is  in  reality  only  very  rarely 
primary,  almost  always  secondary  to  disease  of  neighboring  organs, 
especially  the  lung.  When  cases  are  referred  to  as  primary,  therefore, 
it  should  be  understood  that  the  starting  point  of  the  disease  in 
other  organs  has  not  been  detected.  Throughout  the  sections  on 
effusions,  mention  is  made  of  small,  medium,  and  large  amounts  of 
pleural  fluid.  In  general,  by  "small"  may  be  understood  an  effusion 
which  does  not  rise  above  the  angle  of  the  scapula;  by  "medium," 
an  upper  level  between  the  angle  and  spine  of  the  scapula,  and  by 
"large,"  a  higher  level. 


ACUTE  FIBRINOUS  PLEURITIS. 

Fibrinous  or  Plastic  Pleuritis. — The  examination  of  cases  with  fibrin- 
ous pleuritis  at  the  postmortem  table  shows  that  small  amounts  of 
fluid  are  usually  present.  From  its  clinical  importance,  however,  the 
group  deserves  separate  consideration. 

Etiology. — The  absence  of  fluid  for  examination  makes  the  etiology 
of  fibrinous  pleuritis  somewhat  less  certain  than  the  other  forms, 
but  the  cases  fall  into  two  principal  groups,  those  in  which  the  disease 
is  apparently  (1)  primary  and  those  (2)  secondary  to  disease  of  the 
lung  or  other  part  of  the  body. 

1.  Primary. — This  forms  the  largest  group  in  clinical  cases.  The 
disease  seldom  occurs  in  perfectly  healthy  individuals,  and  some 
disturbance  of  the  respiratory  tract  may  precede,  but  more  often 
accompanies,  the  stitch  in  the  side.  In  this  series,  223  (64.6  per  cent.) 
of  345  cases  may  be  regarded  as  belonging  to  this  class.  Exposure  was 
a  possible  contributing  factor  in  30  and  alcoholism  may  have  played 
a  part  in  19  cases.  The  clinical  history  and  subsequent  course  of 
primary  dry  pleurisy  indicate  that  it  is  due  to  tuberculosis  in  the  vast 
majority  of  the  cases. 

2.  Secondary. — The  disease  may  be  secondary  to  infective  processes 
in  any  part  of  the  body.  Disease  of  the  lung  occupies  first  place  and 
bronchitis  is  an  important  factor.  It  is  probable  that  small  areas  of 
pulmonary  invasion,  too  small  to  be  detected  on  physical  examina- 
tion, frequently  accompany  bronchitis,  and  that  bacteria  find  their 
way  from  the  peripheral  parts  of  the  lung  to  the  pleura.  Infection  with 
the  tubercle  bacillus,  especially  in  the  lung  or  bronchial  lymph  glands, 
may  be  regarded  as  the  starting  point  of  pleural  infection  in  a  large 
proportion  of  cases.  In  this  series  there  was  probable  or  certain  pul- 
monary tuberculosis  in  18  cases  (5.2  per  cent.),  of  which  6  showed 
tubercle  bacilli  in  the  sputum.  The  lung  was  involved  in  16,  tuber- 
culous peritonitis  was  present  in  1,  and  an  anal  fistula  in  the  remaining 
patient.  Lobar  pneumonia  is  a  frequent  cause  and  is  represented  by 
15  cases.  Bronchopneumonia,  abscess,  gangrene,  and  bronchiectasis 
are  less  frequent  causes.      Of  infections  in  more  remote  parts  of  the 


460  DISEASES  OF  THE  PLEURA 

body  may  be  mentioned  acute  or  chronic  endocarditis,  tonsillitis, 
pyorrhea  alveolaris,  arthritis,  pericarditis,  typhoid  fever,  and  uterine 
sepsis.  Dry  pleurisy  is  not  infrequent  in  the  later  stages  of  all  chronic 
diseases  accompanied  by  asthenia  and  increased  susceptibility  to 
infection.  Trauma  with  or  without  gross  injury  of  the  tissues  may 
lead  to  fibrinous  pleuritis  and  usually  by  infection  from  the  lungs. 
Pulmonary  infarction  is  an  occasional  cause.  If  the  venous  throm- 
bosis is  latent  and  hemoptysis  does  not  occur  the  pleurisy  may  be 
regarded  as  primary. 

Relation  to  Tuberculosis. — The  frequency  with  which  pulmonary 
tuberculosis  begins  with  and  is  accompanied  by  symptoms  referable 
to  the  pleura  gives  ample  testimony  of  its  important  relationship. 
Of  1000  cases  in  the  Winyah  Sanatorium,  201  had  pleurisy  prior  to 
the  onset  of  pulmonary  tuberculosis  (von  Ruch) .  Although  the  apical 
localization  of  these  changes  is  most  frequent,  pulmonary  tuberculosis 
is  often  accompanied  by  similar  processes  in  other  parts  of  the  pleura. 
Acute  fibrinous  pleuritis  may  occur  and  tubercles  may  be  found  in 
the  tissue. 

The  proportion  of  cases  in  which  the  tubercle  bacillus  is  responsible 
for  fibrinous  pleuritis  cannot  be  definitely  stated.  A  study  of  my 
cases  suggests  that  this  form  of  pleuritis  as  an  apparently  primary 
affection  is  tuberculous  in  about  the  same  proportion  of  cases  as  in 
primary  serofibrinous  pleuritis.  This  seems  to  be  indicated  by  the  sub- 
sequent course.  (See  Prognosis,  p.  465.)  It  should  be  noted,  however, 
that  coincident  tuberculosis  was  demonstrated  in  a  smaller  proportion 
of  cases  of  fibrinous  (5  per  cent.)  than  of  serofibrinous  pleuritis  (13 
per  cent.),  but  this  may  have  been  due  to  the  fact  that  the  pulmonary 
process  was  in  a  less  advanced  stage. 

Although  the  tubercle  bacillus  may  be  equally  responsible  for  fibrin- 
ous and  serofibrinous  pleuritis,  there  is  some  indication  that  a  mixed 
infection  with  other  organisms  is  more  frequent  in  the  former.  An 
abundant  fibrinous  exudate  is  not  typical  of  infection  with  the  tubercle 
bacillus  alone.  The  behavior  of  the  white  count  is  also  suggestive  of 
mixed  infection,  being  above  12,000  in  19  (39.5  per  cent.)  of  48  cases 
of  primary  fibrinous  pleuritis,  while  only  3  (9.09  per  cent.)  of  33  cases 
of  primary  serofibrinous  effusion,  known  to  be  tuberculous,  exceeding 
this  figure. 

Pathology. — The  inflamed  pleura  lacks  its  normal  lustre,  is  dull, 
opaque,  and  coarsely  or  finely  granular,  an  appearance  which  can 
best  be  seen  by  scraping  the  tissue  with  the  knife.  It  is  grayish-white, 
or  reddish,  and  deeper  red  in  places  where  ecchymoses  are  present. 
The  membrane  is  thickened  and  may  reach  a  centimeter  or  more  in 
width.  The  surface  of  an  abundant  exudate  may  be  thrown  into  folds 
or  projecting  masses  of  various  shapes.  The  amount  of  exuded  liquid 
varies.  There  is  practically  always  more  than  the  normal  amount  of 
pleural  fluid  and  this  is  usually  cloudy.  The  extent  of  pleural  involve- 
ment varies  from  a  part  to  the  whole  of  the  pleura.    It  is  not  uncom- 


ACUTE  FIBRINOUS  PLEURITIS  461 

mon  to  find  some  extension  of  the  inflammation  along  the  interlobular 
septa  in  cases  with  severe  fibrinous  pleuritis. 

On  microscopic  examination,  desquamation  and  degeneration  or 
absence  of  epithelial  cells  are  found.  The  subserous  tissue  is  swollen 
and  contains  an  increased  number  of  polynuclear  cells.  Lymph  and 
bloodvessels  are  widened.  The  surface  of  the  pleura  is  the  site  of  a 
fibrinous  layer  containing  numerous  piis  cells  and  serum.  With  the 
beginning  of  resolution  the  fibrin  undergoes  fatty  metamorphosis  and 
in  mild  cases  may  entirely  disappear.  In  more  severe  inflammations 
the  two  lasers  of  pleura  become  adherent.  Organization,  round-celled 
infiltration,  and  connective-tissue  formation  take  place,  giving  rise 
to  adhesive  pleuritis. 

Site. — This  is  variable,  but  the  process  is  most  often  discovered 
clinically  in  the  lower  lateral  and  anterior  aspects  of  the  chest.  This 
is  due  to  the  more  frequent  occurrence  of  fibrinous  pleuritis  at  the 
bases,  the  greater  respiratory  excursion  of  the  lower  part  of  the  lung, 
increasing  the  loudness  of  friction  sound,  and  the  relative  thinness  of 
the  thoracic  wall,  facilitating  the  detection  of  pleural  processes  here. 
The  more  frequent  discovery  of  pleural  friction  in  the  lateral  and 
anterior  rather  than  in  the  posterior  part  of  the  chest  may  be  due  also 
to  the  tendency  of  small  amounts  of  fluid  to  collect  at  the  base  posteri- 
orly, with  mechanical  limitation  of  pulmonary  motion  and  slight 
intervention  of  fluid  between  lung  and  chest  wall  in  this  region.  Of 
323  cases  in  which  the  site  of  the  process  was  noted  in  this  series,  it 
was  on  the  right  in  134  patients,  in  131  on  the  left,  while  the  process  was 
limited  to  the  right  upper  chest  in  20,  to  the  left  upper  chest  in  9.  Of 
the  remaining  29  cases,  a  situation  at  both  bases  in  7,  in  the  diaphrag- 
matic pleura  in  3,  and  throughout  the  left  side  in  1  may  be  mentioned. 

Symptoms. — Prodromata  are  relatively  uncommon.  Cough  and 
expectoration,  due  to  respiratory  infection,  may  precede  the  stitch 
in  the  side.  In  a  majority  of  the  cases  the  onset  is  sudden,  with  pain, 
which  varies  much  in  intensity.  An  initial  chill  is  rare.  The  tempera- 
ture is  often  not  elevated  and  was  not  above  normal  in  82  (23.7  per 
cent.)  of  345  cases.  A  temperature  of  99°  to  100°  or  101°  is  not  uncom- 
mon. It  may  rise  to  103°  or  higher,  but  high  temperature  is  more 
often  seen  in  complicated  cases.  Fever,  usually  gradually  subsides 
within  a  few  days. 

Pain. — Pain  is  an  almost  constant  feature.  It  may  be  absent  after 
the  acute  symptoms  have  subsided  or  at  the  extremes  of  age.  It  is 
often  described  as  sharp,  stabbing,  or  cutting,  sometimes  dull  and 
dragging  in  character.  It  is  usually  circumscribed,  rarely  diffuse, 
and  is  felt  in  the  axillary  or  mammary  region,  less  commonly  in  the 
anterior  or  posterior  lateral  and  lower  parts  of  the  affected  chest. 
It  may  radiate  to  the  shoulder  or  lumbar  region,  less  commonly  into 
the  upper  extremity,  the  neck  or  abdomen.  The  rare  cases  in  which 
the  pain  is  at  first  referred  to  the  abdomen  are  troublesome  for  diag- 
nosis.   Of  145  cases  in  this  series  this  occurred  in  8  (5.5  per  cent.), 


162  DISEASES  OF   THE  PLEURA 

and  may  have  been  due  to  diaphragmatic  pleurisy.    Pleuritic  friction 

may  be  absent  and  the  case  may  then  present  the  picture  of  an  acute 
abdominal  affection.  The  pain  is  usually  in  the  upper  abdominal 
region.  It  may  be  accompanied  by  tenderness  and  muscular  spasm 
and  suggest  ah  inflammatory  abdominal  condition.  Indeed,  laparo- 
tomy has  occasionally  been  performed  in  cases  in  which  a  few  days 
later  the  pleuritic  origin  of  the  symptoms  became  obvious  from  the 
presence  of  friction  or  effusion.  Capps1  explored  the  pleural  cavity 
by  means  of  a  wire  passed  through  the  cannula  of  an  instrument  for 
thoracentesis.  The  visceral  pleura  seemed  devoid  of  pain  sense. 
Irritation  of  the  parietal  pleura  gave  rise  to  pain  over  the  site  of  irri- 
tation. Irritation  of  the  central  portion  of  the  diaphragmatic  pleura 
caused  pain  in  the  neck,  of  maximum  intensity  along  the  ridge  of  the 
trapezius  muscle  (fourth  spinal  segment).  Irritation  of  the  peripheral 
rim  of  the  diaphragmatic  pleura  elicited  pain  in  the  lower  thorax, 
the  lumbar  region  or  the  abdomen. 

The  pain  of  fibrinous  pleuritis  is  usually  of  moderate  intensity, 
at  times  almost  unbearable,  at  others  slight,  and  present  only  with 
long  breath  or  cough.  It  may  be  continuous  or  intermittent,  but  is 
usually  most  marked  at  the  beginning  of  the  illness,  disappearing  sud- 
denly or  gradually  within  a  week  to  ten  days.  In  some  cases  it  may 
last  for  weeks  or  months.  Movement,  laughter,  pressure  on  or  percus- 
sion of  the  affected  side,  quick  change  of  position,  even  elevation  of  the 
arm,  may  start  or  aggravate  it.  With  the  advent  of  pleural  effusion, 
pain  diminishes  or  disappears.  The  cause  of  pain  in  pleural  disease 
is  uncertain.  It  is  probably  due  to  irritation  of  terminal  nerve  fila- 
ments in  the  inflamed  tissue. 

Cough.—  This  is  present  in  a  large  proportion  of  cases.  Of  145 
patients  it  was  noted  in  103  (71  per  cent.).  It  was  stated  to  be  absent 
in  18,  a'nd  the  records  are  silent  on  this  point  in  24.  It  is  usually 
ascribed  to  pleural  irritation,  and  a  relation  with  this  is  suggested  by 
the  frequency  with  which  forced  respiration  excites  cough,  and  by 
its  relief  when  the  side  is  immobilized.  Experimentation  in  animals 
has  failed  to  confirm  this  supposition,  but  it  may  be  that  animals 
are  less  susceptible  to  pleural  irritation.  It  is  probable  that  pulmonary 
infection  plays  a  part  in  its  production,  for  in  44  cases  (30.3  per  cent.) 
expectoration  accompanied  the  cough  and  rales  were  noted  in  45 
(31  per  cent.).  The  sputum  lacks  characteristic  features.  It  was 
mucopurulent  or  purulent  in  many.    In  G  cases  it  was  bloody. 

Dysjmea. — Quick  respiration  may  exist  without  dyspnea.  When 
it  occurs,  dyspnea  is  usually  slight.  It  may  be  due  to  fever,  an  effort 
on  the  part  of  the  patient  to  limit  the  excursion  of  the  lung,  because 
of  pain,  or  to  encroachment  on  pulmonary  space  by  an  effusion. 

Physical  Signs. — The  position,  if  confined  to  the  bed,  is  inconstant; 
at  times  some  relief  is  afforded  by  lying  on  the  affected  and  at  other 

1  Trans.  Assoc.  Amer.  Phys.,  1910,  xxvi,  486. 


ACUTE  FIBRINOUS  PLEUBITIS  463 

times  on  the  unaffected  side.  The  patient  is  often  more  comfortable 
with  the  upper  part  of  the  spine  deflected  toward  the  diseased  pleura 
and  the  shoulder  of  that  side  depressed,  from  the  fixation  and  compres- 
sion which  this  position  affords.  A  diminished  expansion  and  elevation 
of  the  involved  side  can  be  seen  as  well  as  felt,  most  often  in  the  lower 
lateral  thoracic  region.  The  pulmonary  excursion,  as  shown  by  per- 
cussion of  the  lower  pulmonary  margin  at  the  end  of  inspiration  and 
expiration,  and  by  the  amplitude  of  the  diaphragm  phenomenon, 
is  usually  diminished  for  both  lungs,  much  diminished  or  absent  on 
the  affected  side,  and  the  interspaces  are  slightly  narrower.  Percus- 
sion may  be  painful.  A  change  in  the  percussion  note  may  be 
determined.  The  respiratory  murmur  is  diminished  but  vesicular 
in  character;  the  vocal  fremitus  may  be  diminished,  but  is  usually 
unchanged. 

Pleuritic  Friction. — A  friction  rub  can  be  heard  and  not  infrequently 
felt  as  early  as  twelve  to  twenty-four  hours  after  the  onset.  Its 
occurrence  and  resemblance  to  the  creaking  of  leather  did  not  escape 
Hippocrates.  It  is  often  jerky  and  may  be  inconstant,  present  during 
one,  absent  at  the  next  respiration,  such  irregularity  being  due  to 
alternate  fixation  and  motion  of  the  visceral  against  the  parietal 
pleura.  It  may  disappear  during  the  course  of  the  examination.  The 
rub  is  more  distinct  during  inspiration  than  expiration.  Fibrinous 
pleuritis  may  exist  without  friction  sound,  and  friction  does  not 
exclude  fluid  in  a  neighboring  part  of  the  pleura.  The  sound  is  not 
pathognomonic  of  pleuritis. 

Pseudopleiiritic  Friction. — Students  frequently  confuse  with  pleural 
friction  a  sound  often  heard  over  the  back  in  normal  individuals. 
This  sound  is  commonly  heard  during  the  examination  of  the  pos- 
terior thoracic  region  while  the  patient's  arms  are  folded  across  the 
chest,  each  hand  resting  on  the  opposite  shoulder.  It  does  not  usually 
appear  at  once  and  may  be  present  only  after  two  or  more  minutes 
of  forced  respiration.  It  begins  as  an  inconstant,  rumbling,  grating 
sound,  at  first  confined  to  inspiration,  becoming  more  and  more  intense 
and  finally  occupying  both  phases  of  respiration.  It  may  be  harsh 
and  hardly  to  be  distinguished  by  quality  alone  from  pleuritic  friction. 
A  variation  in  intensity  may  be  noted  in  different  patients  and  in  the 
course  of  the  examination  of  the  same  patient,  ordinarily  increasing 
for  a  time  and  then  gradually  fading  away.  It  may  be  reproduced 
after  an  interval  of  quiet  and  heard  in  subsequent  examinations.  It 
is  usually  bilateral.  At  times  it  can  be  felt  with  the  hand  and  may  be 
audible  several  inches  from  the  side.  The  patient  may  appreciate  it 
as  a  grating  sensation  but  it  causes  no  pain.  In  the  back  it  is  confined 
to  the  scapular  region  and  may  be  followed  upward  to  a  point  of 
maximum  intensity  over  the  shoulder-joint.  At  times  it  can  be  heard 
along  the  clavicle  and  down  the  arms  as  far  as  the  hand.  Removal 
of  the  hands  from  the  shoulders  may  abolish  it.  The  sound  is  due  to 
crepitus  at  the  shoulder-joint.     It  is  rougher  than  the  sound  heard 


464  DISEASES  OF   THE  PLEURA 

over  any  contracting  muscle  of  the  extremities  and  is  not  to  be  regarded 
as  a  muscle  sound.  Its  less  jerky  character,  bilateral  position  over 
the  scapulae,  maximum  intensity  over  the  shoulder-joint,  disappearance 
on  shifting  the  arms  and  the  absence  of  pain  serve  to  distinguish  it 
from  pleuritic  friction. 

Pleuroperieardial  Friction. — This  is  not  infrequent  and  is  often 
difficult  of  interpretation.  It  may  be  due  to  inflammation  of  the 
pulmonary,  costal,  or  that  part  of  the  mediastinal  pleura  overlying 
the  heart.  It  is  Jikely  to  be  influenced  by  the  movement  of  the  heart 
as  well  as  by  respiration.  Owing  to  the  variable  line  of  reflection  of 
the  left  costal  pleura  over  the  cardiac  region,  a  distinction  between 
pericardial  and  extrapericardial  friction  cannot  always  be  safely  made 
from  its  situation  alone,  but  in  general  it  may  be  said  that  pleuro- 
perieardial friction  is  uncommon  over  the  superficial  cardiac  dulness, 
and  is  usually  heard  outside  this  region.  It  is  influenced  more  than 
pericardial  friction  by  the  respiratory  movements.  If  the  patient 
stops  breathing,  the  friction  sound  may  diminish  or  disappear. 

Pseudopleural  Intrapulmonary  Sounds. — Loud  sonorous  rales  may 
occasionally  simulate  pleural  friction.  Their  less  jerky  character  and 
disappearance  after  cough  may  suggest  their  pulmonary  origin. 

Pleural  Crepitation. — At  times  with  symptoms  of  pleuritis,  fine,  in- 
spiratory crepitations  are  heard  over  the  site  of  the  suspected  process. 
These  may  be  pleural  in  origin,  but  can  hardly  be  differentiated  from 
intrapulmonary  rales. 

Blood. — White  Cells. — Fibrinous  pleuritis  is  more  often  accompanied 
by  leukocytosis  than  serofibrinous  pleuritis.  Thus,  of  48  cases  of 
primary  fibrinous  pleuritis,  the  white  count  was  12,000  or  over  in  19 
(39.5  per  cent.).  Of  these  19  cases,  the  white  cells  numbered  12,000 
to  13,000  in  3;  from  13,000  to  14,000  in  4;  14,000  to  15,000  in  4; 
15,000  to  16,000  in  2;  16,000  to  20,000  in  3,  and  20,000  to  24,000 
in  3.  The  difference  between  the  white  count  in  primary  fibrinous  and 
that  in  primary  tuberculous  serofibrinous  pleuritis  is  quite  striking 
in  my  small  series  of  cases,  only  3  of  33  cases  in  the  latter  group 
showing  12,000  or  more  white  cells. 

Sequelae. — Of  345  cases,  pleural  fluid  was  discovered  as  a  sequence 
of  the  process  in  5. 

Diagnosis. — This  is  usually  easily  made  from  the  presence  of  a  friction 
rub.  Cases  with  an  acute  onset,  with  cough  and  stitch  in  the  side, 
aggravated  by  respiration,  are  due  to  pleuritis  in  a  large  proportion 
of  the  cases,  even  if  no  friction  rub  can  be  heard.  The  diagnosis  of 
diaphragmatic  pleurisy  is  often  troublesome  and  may  remain  in  doubt 
for  several  days.  Cases  in  which  pain  along  the  lower  thoracic  margin 
is  the  only  symptom  are  most  difficult  of  diagnosis.  To  judge  from 
the  remarkable  frequency  with  which  there  is  postmortem  indication 
of  previous  disease  of  the  pleura,  it  is  probable  that  an  undetected 
pleurisy  is  the  cause  in  a  large  proportion  of  the  cases.  Rarely  the 
pain  is  the  precursor  of  herpes  zoster.     Pulmonary  embolism  from 


ACUTE  FIBRINOUS  PLEURITIS  465 

venous  thrombosis  should  always  be  considered  as  a  possible  cause 
of  an  apparently  primary  dry  pleurisy.  Phlebitis  of  the  veins  of  the 
extremities  is  not  always  manifest  and  the  embolus  may  come  from 
a  pelvic,  abdominal  or  thoracic  vein.  The  possibility  of  spinal  disease 
must  be  borne  in  mind.  Tertiary  syphilis  and  tumor  are  to  be  con- 
sidered. Lead  poisoning,  caries  of  the  ribs,  periostitis,  and  thoracic 
aneurysm  should  be  excluded.  The  .i-rays  may  help  in  the  diagnosis. 
A  diagnosis  of  pleurodynia  or  intercostal  neuralgia  amounts  to  a  con- 
fession of  ignorance  concerning  the  cause  of  the  process. 

In  typical  cases  there  is  little  danger  of  confusion,  but  the  signs 
may  be  those  of  thickened  pleura,  dulness,  diminished  vesicular 
breathing,  with  preservation  of  the  fremitus,  even  a  friction  rub,  and 
yet  fluid  may  be  present.  The  fluid  may  exist  between  lung  and 
diaphragm,  where  small  amounts  are  likely  to  collect  first,  and  rise 
little  above  the  pulmonary  margin  between  lung  and  chest  wall.  In 
other  cases  there  may  be  evidence  of  thickened  pleura  and  oftenest 
in  the  lower  anterior  aspect  of  the  chest,  with  fluid  in  the  posterior, 
inferior  thoracic  region.  Again,  fluid  may  be  encapsulated  and 
fibrinous  pleuritis  with  friction  coexist.  In  doubtful  cases  an  explora- 
tory puncture  must  be  made.  Cases  with  complicating  pulmonary 
disease  are  likely  to  cause  most  difficulty  in  diagnosis. 

Primary  dry  "pleurisy  should  be  regarded  as  probably  tuberculous  in 
origin.  Preceding  good  health,  satisfactory  general  condition  and 
mild  symptoms  during  the  attack  are  not  to  be  regarded  as  sufficient 
evidence  against  this  diagnosis.  Primary  dry  pleurisy,  as  an  indica- 
tion of  tuberculosis,  is  equal  in  significance  to  primary  pleurisy  with 
serofibrinous  effusion  or  hemoptysis  out  of  a  clear  sky. 

Prognosis. — Th'e  immediate  outlook  in  fibrinous  pleuritis  is  good. 
The  more  remote  prospects  are  less  favorable.  Of  82  cases  of  primary 
dry  pleurisy  in  my  series1  60  have  been  followed  since  their  discharge 
from  the  hospital.  Of  these,  18  (30  per  cent.)  certainly  or  probably 
developed  tuberculosis.  Their  subsequent  course  has  been  followed 
from  one  to  twelve  years,  the  average  interval  being  four  or  five  years. 
The  outcome  of  primary  dry  pleuritis  is  thus  nearly  or  quite  as  bad 
as  that  of  primary  serofibrinous  effusion.  The  prognosis  of  the  secon- 
dary form  is  that  of  the  underlying  cause.  Pain  may  persist  after  the 
attack;  15  patients  (25  per  cent.)  complain  of  occasional  or  persistent 
pain. 

Treatment. — The  immediate  indication  is  the  relief  of  pain,  on  which 
the  cough  and  dyspnea  largely  depend.  Rest  is  the  first  consideration. 
In  all  cases  in  which  there  is  fever  or  severe  pain,  the  patient  should 
be  in  bed.  Even  in  mild  attacks,  rest  shortens  the  duration  and  may 
prevent  extension  or  the  occurrence  of  an  effusion. 

Fixation  of  the  side  limits  the  play  of  the  pulmonary  against  the 
parietal  pleura  and  may  produce  immediate  relief.    It  may  be  accom- 

1  Lord,  Boston  Med.  and  Surg.  Jour.,  April  15,  1909. 
30 


466  DISEASES  OF   THE  PLEURA 

plished  with  adhesive  plaster,  of  which  zinc  oxide  plaster  is  best.    One 

end  of  a  strip  of  well-warmed  adhesive  plaster,  the  width  of  the  hand 
and  long  enough  to  reach  from  the  spine  to  the  sternum,  is  applied 
against  the  paravertebral  region.  The  operator  then  forcibly  wraps 
the  strip  about  the  lower  thoracic  region  so  that  it  lies  stretched  over 

the  lower  ribs,  and  thus  limits  their  excursion.  In  women  with  pen- 
dulous breasts,  several  narrow  strips  of  plaster,  extending  from  the 
paravertebral  region  downward  and  forward,  from  the  sternum 
downward  and  backward  and  intersecting  in  the  axillary  region,  may 
be  more  comfortable.  The  plaster  should  not  be  allowed  to  remain 
longer  than  a  week  to  ten  days,  and  care  taken  in  its  removal  not  to 
cause  abrasion  of  the  skin.  A  tight  thoracic  swathe,  with  shoulder 
and  peroneal  straps,  has  the  advantage  of  ready  removal  for  physical 
examination,  and  does  not  lead  to  irritation  or  infection  of  the  skin. 
It  is  to  be  preferred  for  patients  in  bed.  In  some  cases,  perhaps  from 
diaphragmatic  involvement,  fixation  of  the  thorax  fails  to  give  relief. 
In  such  cases  an  ice-bag  or  hot-water  bottle  may  be  efficient.  If 
these  means  fail,  a  hypodermic  injection  of  morphin  may  be  given. 

A  possible  source  of  infection  should  be  sought,  and  if  found  in  any 
part  of  the  body,  should  receive  appropriate  treatment.  The  occur- 
rence of  dry  pleuritis  should  always  suggest  the  possibility  of  tuber- 
culosis. The  chance  of  this  is  much  increased  by  a  family  history  of 
the  disease  or  opportunity  for  contagion.  Careful  examination  of 
the  lungs,  the  sputum,  and  the  use  of  tuberculin  may  furnish  positive 
or  suggestive  evidence. 

All  cases  of  primary  fibrinous  pleurisy,  even  the  mildest  forms,  in 
patients  otherwise  in  apparent  health,  should  be  treated  as  if  tubercu- 
lous until  the  pleuritis  can  be  proved  to  be  due  to  another  cause.  The 
best  results  in  most  instances  can  be  obtained  only  when  the  patient 
is  frankly  told  the  probable  seriousness  of  his  trouble  and  the  danger 
if  untreated  of  developing  more  extensive  tuberculosis.  He  can  other- 
wise hardly  be  expected  to  undergo  the  necessary  restrictions  on  his 
mode  of  life.  The  inability  to  make  more  than  a  probable  diagnosis 
of  tuberculosis  in  the  primary  dry  pleurisies  without  fluid  for  examina- 
tion should  not  be  allowed  to  act  to  his  detriment.  The  later  histories 
clearly  showT  how  imminent  the  danger  is  and  that  hesitation  and 
delay  may  bring  him  a  second  time  under  observation  with  the  disease 
too  advanced  for  successful  treatment. 

The  general  management  of  suspected  or  proved  pleural  tuberculosis 
may,  in  brief,  be  considered  to  be  the  same  as  that  for  incipient  or 
manifest  pulmonary  tuberculosis.  Rest,  fresh  air,  and  extra  feeding 
are  of  chief  importance.  Mild  cases  of  simple  dry  pleurisy  can  often 
sufficiently  modify  their  surroundings  to  make  "home"  treatment  a 
success,  but  the  necessity  for  discontinuance  or  change  of  occupation, 
removal  to  more  favorable  quarters,  choice  between  treatment  at 
home,  in  a  tuberculosis  class,  or  in  a  sanitarium  can  be  decided  only 
after  careful  consideration  of  the  circumstances  in  each  case. 


ACUTE  SEROFIBRINOUS  PLEURITIS  407 

The  physician's  responsibilities  do  not  end  with  the  apparently 
favorable  outcome  of  the  acute  attack.  No  matter  how  mild  this 
has  been  or  how  reassuring  the  general  condition  appears  to  be,  per- 
manent results  can  be  attained  only  by  supervision  at  regular  intervals 
and  instruction  to  report  at  once  on  the  occurrence  of  another  attack, 
failing  health,  rise  of  temperature  or  other  suspicious  symptoms. 

ACUTE   SEROFIBRINOUS   PLEURITIS. 

Etiology. — Serofibrinous  effusions  arising  from  inflammation  of  the 
pleural  sac  may  be  divided  into  three  principal  groups:  (1)  Tubercu- 
lous pleuritis  comprises  the  largest  and  most  important  division.  (2) 
Infectious  (non-tuberculous)  pleuritis  stands  next  in  frequency  and  is 
a  well-defined  class.  (3)  Other  causes  are  relatively  infrequent  and 
often  difficult  to  group.  They  are  the  product  of  more  than  one  factor, 
such  as  general  hydremia  or  venous  stasis,  on  which  an  inflammatory 
process  is  superimposed. 

1.  Tuberculous  Pleuritis. — It  is  remarkable  in  how  many  cases 
serofibrinous  pleuritis  is  apparently  primary  without  evidence  of 
disease  in  other  organs.  Thus  of  1185  cases  the  disease  of  the  pleura 
was  unassociated  with  positive  findings  elsewhere  in  750  (63.4  per 
cent.).  The  pleural  disease  was  combined  with  suggestive  or  positive 
evidence  of  pulmonary  or  other  tuberculosis  in  160  (13.5  per  cent.). 
The  lung  was  the  most  frequent  site  of  tuberculosis  in  this  group  with 
149  cases,  of  which  47  showed  tubercle  bacilli  in  the  sputum.  Tubercu- 
lous peritonitis  was  present  in  9  and  tuberculosis  in  other  regions  in 
2  patients. 

There  is  good  reason  to  believe  that  a  large  proportion  of  cases  of 
serofibrinous  effusion,  more  especially  the  primary  cases  and  those 
secondary  to  pulmonary  tuberculous  lesions,  are  due  to  tuberculosis. 
This  point  of  view  is  largely  the  result  of  recent  investigations  and 
is  based  on  the  following: 

(a)  Tuberculosis  of  Other  Organs. — In  Osier's  195  cases,  30  showed 
tubercle  bacilli  in  the  sputum.  Pleural  effusion  as  a  symptom  of 
pulmonary  tuberculosis  usually  comes  early  if  at  all.  Dense  pleural 
adhesions  commonly  obliterate  part  or  the  whole  of  the  pleural  sac  in 
an  advanced  stage  of  the  disease. 

(b)  The  Subsequent  History. — The  after  histories  of  130  cases  of 
primary  pleurisy  with  effusion  by  Hedges1  showed  that  at  least  40 
per  cent,  died  of  or  had  tuberculosis  within  six  years.  Osier2  refers 
to  86  cases  of  which  34.8  per  cent,  became  tuberculous  and  died, 
while  Sokolowski3  followed  26  cases  for  six  years.  Of  Sokolowski's 
cases,  10  (38  per  cent.)  developed  tuberculosis.  The  subsequent 
course  of  90  cases  of  primary  pleurisy,  irrespective  of  its  type,  was 

11  St.  Bartholomew's  Hosp.  Rep.,  1900,  xxxvi,  83. 

2  British  Med.  Jour.,  October  15,  1904. 

3  Klinik  der  Brustkrankheiten,  1906. 


468  DISEASES  OF  THE  PLEURA 

investigated  by  V.  Y.  Bowditch.a  Of  this  scries,  32  (35  per  cent.) 
died  of  or  had  phthisis.  Sears2  followed  a  similar  series  from  the 
records  of  the  Boston  City  Hospital  to  the  state  archives  and  found 
that  of  86  known  to  have  died  the  cause  was  some  form  of  tuberculosis 
in  over  55  per  cent. 

(c)  Postmortem  Evidence. — Of  131  cases  of  different  types  of  pleu- 
ritis  examined  postmortem  by  Osier,  32  were  found  to  be  definitely 
tuberculous. 

(d)  The  Tuberculin  Reaction. — This  is  positive  in  a  large  proportion 
of  the  cases — in  7.">.7  per'  cent,  of  Beck's  series  and  in  7  of  8  cases  by 
F.  W.  White.  In  my  series  (M.  G.  H.)  tuberculin  was  given  in  47; 
36  (76.5  per  cent.)  gave  a  positive  reaction.  A  positive  result  merely 
means  tuberculosis  somewhere,  not  necessarily  in  the  pleura. 

(e)  The  Character  of  the  Exudate. — The  evidence  is  based  on  the 
character  of  the  cells,  the  demonstration  of  tubercle  bacilli  in  the  fluid, 
and  the  results  of  animal  inoculation. 

Character  of  the  Cells. — Lymphocytes  predominate  in  a  large  propor- 
tion of  serofibrinous,  fluids  from  patients  known  to  have  tuberculosis 
of  the  pleura;  they  are  likewise  in  excess  in  cases  in  which  pulmonary 
tuberculosis  is  certainly  or  probably  present,  and  the  same  cellular 
formula  is  present  in  idiopathic  pleurisy  with  effusion.  Excess  of 
lymphocytes  is  not  invariably  proof  of  a  tuberculous  pleurisy. 

Tubercle  Bacillus  in  the  Fluid. — The  effort  to  cultivate  tubercle 
bacilli  from  serous  effusions  practically  always  fails.  Simple  micro- 
scopic examination  likewise  is  usually  unsuccessful.  Of  415  cases 
collected  by  Xetter  from  various  sources,  bacilli  wrere  found  in  only  9 
(about  2  per  cent.).  Inoscopy  or  sedimentation  has  given  more  posi- 
tive results.  In  primary  cases,  Jousset  claimed  by  means  of  inoscopy 
to  have  found  tubercle  bacilli  in  23  cases  (100  per  cent.),  but  other 
observers  have  failed  to  confirm  his  results.  In  115  cases  at  the 
Massachusetts  General  Hospital  in  which  tubercle  bacilli  were  sought 
in  the  fluid,  they  were  found  in  24  (20.8  per  cent.).  Kormoczi  and 
Jassniger3  found  bacilli  in  3  of  8  cases.  Zebrowski,4  by  simple  sedimen- 
tation of  a  large  quantity  of  fluid,  prevented  from  coagulation  by  the 
addition  of  sodium  fluoride,  found  bacilli  in  12  (55  per  cent.)  of  22 
primary  cases  and  in  10  (83  per  cent.)  of  12  secondary  effusions. 

Animal  Inoculation. — The  most  convincing  evidence  is  obtained 
by  animal  inoculation.  Of  66  cases  in  my  series  the  results  were 
positive  in  15  (22.7  per  cent.).  Aschoff,5  using  3  c.c.  of  fresh  exudate, 
obtained  positive  results  in  9  (75  per  cent.)  of  12  cases;  Eichorst6 
with  15  c.c.  in  65.2  per  cent,  of  23;  and  Le  Damany,7  by  the  inocula- 
tion of  10  to  50  and  at  times  as  much  as  300  c.c,  in  all  but  8  (85  per 

1  Trans.  Amer.  Climat.  Assoc,  18S9,  vi,  1-13. 

2  Boston  Med.  and  Surg.  Jour.,  1904,  cl,  209. 

3  Deut.  med.  Woch.,  1904,  p.  342.  4  Ibid.,  1905,  No.  36. 
s  Zeit.  f.  klin.  Med.,  1896,  xxix,  440. 

6Cor.-BI.  f.  Schw.  Aerzte,  1895,  xxv,  385. 
7  Presse  med.,  November  24,  1897. 


ACUTE  SEROFIBRINOUS  PLEURITIS  469 

cent.)  of  55  primary  cases,  while  in  4  of  the  8  negative  cases  coincident 
lesions  indicated  their  tuberculous  origin.  Repeated  intraperitoneal 
injections  of  from  10  to  50  c.c.  were  made  each  week.  It  should  be 
remembered  that  human  as  well  as  horse  serum  is  capable  of  sensiti- 
zing guinea-pigs  and  that  repetitions  after  a  longer  interval  may  result 
in  severe  symptoms  of  anaphylaxis  and  in  death  of  the  animal.  It 
is  fair  to  assume  that  the  percentage  is  higher  than  these  figures  show. 
Tubercle  bacilli  may  be  absent  from  the  particular  sample  of  fluid 
investigated,  or  postmortem  examination  of  animals  at  too  short  an 
interval  may  introduce  a  small  error.  In  rare  instances  glandular 
lesions  which  can  be  conclusively  demonstrated  as  tuberculous  only 
after  microscopic  examination  of  stained  sections  may  be  observed 
in  animals  six  weeks  after  inoculation.  It  is  safer  therefore  to  inoculate 
more  than  one  animal  and  to  sacrifice  only  the  manifestly  tuberculous 
animals  after  the  customary  interval  of  six  weeks  and  to  allow  others 
to  live  for  three  months. 

By  the  presence  of  tubercle  bacilli  in  the  sputum,  in  the  fluid  by 
animal  inoculation  or  inoscopy,  or  by  operation,  Musgrave  proved 
the  tuberculous  character  of  28  (54.9  per  cent.)  of  51  primary  or 
secondary  effusions. 

There  can  be  no  doubt  from  these  considerations  that  tuberculosis 
occupies  first  place  in  the  etiology  of  pleural  effusions  in  any  large 
series  of  cases.  When  such  cases  are  demonstrated  as  tuberculous,  it 
is  probable  that  they  have  been  so  from  their  inception,  and  not  through 
secondary  infection  with  the  tubercle  bacillus,  although  such  an  event 
cannot  be  excluded  as  a  rare  occurrence.  All  serofibrinous  effusions 
cannot  be  classed  as  tuberculous. 

2.  Infectious  (Non-tuberculous)  Pleuritis. — Infection  of  the  pleura 
with  other  organisms  than  the  tubercle  bacillus  is  capable  of  causing 
serofibrinous  effusion.  The  pneumococcus  is  the  most  frequent  cause 
in  this  group.  The  streptococcus  and  other  organisms  may  likewise 
be  a  cause.  A  difficulty  lies  in  the  exclusion  of  the  tubercle  bacillus 
as  a  mixed  infection. 

(a)  Metapneumonic  Pleuritis. — This  is  a  well-defined  group  and  is 
represented  by  62  (5*2  per  cent.)  of  1185  cases  with  serofibrinous 
effusion. 

Small  effusions  of  a  serofibrinous  or  purulent  character  are  common 
in  lobar  pneumonia.  Maragliano  demonstrated  serofibrinous  or 
purulent  effusion  in  38  of  58  cases,  by  means  of  exploratory  puncture. 
If  small  amounts  are  included,  a  serofibrinous  is.  more  common  than 
a  purulent  exudate.  Norris1  in  127  autopsies  in  pneumonia,  found 
serous  in  5  and  purulent  fluid  in  20  cases,  while  Kerr  in  173  autopsies 
found  38  with  serofibrinous  and  6  with  purulent  effusion.  Of  154 
autopsies  on  cases  with  lobar  pneumonia  (M.  G.  H.),  a  pleural  effu- 
sion was  present  in  57,  and  in  these  the  fluid  was  cloudy  in  30,  clear 

1  Osier's  Modern  Medicine,  1907,  ii,  598. 


470  DISEASES  OF  THE  PLEURA 

in  10,  purulent  in  9,  and  hemorrhagic  in  6.  The  largest  amount  at 
autopsy  was  500  c.c.,  and  was  unrecognized  during  life.  The  cloudi- 
ness so  commonly  seen  in  such  effusions  is  usually  due  to  fine  fibrin- 
ous flocculi.  •  Tuberculosis  was  present  in  the  lungs  or  bronchial 
glands  in  9  of  the  cases,  in  6  of  which  it  appeared  to  be  obsolete,  while 
in  1  it  was  a  probable  cause  of  the  effusion.  In  Sello's  cases  the 
effusion  was  demonstrated  at  the  beginning  of  the  pneumonia  in  2, 
during  the  course  of  the  disease  in  31,  and  afterward  in  24.  The 
independent  existence  of  serofibrinous  effusion  accompanying  pneu- 
monia and  due  to  infection  with  other  organisms  than  the  tubercle 
bacillus  cannot  be  doubted.  In  support  of  this  is  its  association  with 
an  inflammatory  disease  of  the  lung,  usually  due  to  the  pneumo- 
coccus,  the  presence  in  the  fluid  of  pneumococci  or  other  organisms 
which  alone  are  capable  of  causing  pleuritis  with  effusion,  and  the 
absence  in  cases  with  serofibrinous  effusion  and  pneumonia  of  tuber- 
culous lesions  at  autopsy. 

(b)  Rheumatism. — This  was  coincident  with  pleuritis  with  effusion 
in  13  cases  (0.9  per  cent.).  There  is  no  proof  that  the  rheumatic 
poison  can  alone  infect  the  pleura,  and  it  seems  misleading  to  speak 
of  a  rheumatic  pleuritis  in  the  sense  in  which  this  term  is  sometimes 
used  to  designate  a  pleuritis  with  or  without  arthritic  symptoms, 
in  which  a  favorable  result  is  obtained  following  the  administration 
of  salicylic  acid  preparations.  Until  proof  can  be  offered  that  rheu- 
matic fever  is  due  to  a  specific  organism,  and  this  can  be  demonstrated 
in  pleural  effusions  as  a  cause,  it  is  better  for  clinical  purposes  to  regard 
such  effusions  as  complicate  arthritis  as  only  possibly  rheumatic  in 
origin.  Infection  of  the  joints  and  the  pleura,  wTith  discovery  of 
streptococci  in  both,  was  associated  with  panophthalmitis  in  one 
case;  in  another  the  joints,  the  pleura,  the  endo-  and  pericardium  were 
simultaneously  involved.  In  both  cases  the  pleural  fluid  showed 
an  excess  of  polynuclear  cells,  viz.,  95  per  cent,  and  65  per  cent., 
respectively.  As  in  other  forms  of  pleuritis,  tuberculosis  must  be 
excluded. 

(c)  Trauma. — Serofibrinous  effusion  followed  trauma  in  10  cases 
(0.8  per  cent.)  in  this  series.  The  effusion  may  be  due  to  simple  infec- 
tion or  to  tuberculosis.  Traumatic  serous  pleuritis  has  been  followed 
by  the  development  of  pulmonary  tuberculosis  (Lebert),  and  tubercle 
bacilli  have  been  found  in  the  fluid  by  Chauffard,  Herbert,  Barjon 
and  Lesier,  and  Chevastelon  (quoted  from  Chevastelon). 

(d)  Typhoid  Fever. — The  association  of  serofibrinous  effusion  and 
typhoid  is  rare,  occurring  in  only  7  cases  (0.5  per  cent.)  in  this  series. 
Among  1500  cases  of  typhoid,  McCrae1  noted  only  3  with  serous 
effusion.  The  bacilli  have  been  obtained  in  pure  culture  from  the 
fluid  by  Fernet,  Achard  and  Gordinier,  and  Lartigau.  In  Achard's 
case  the  fluid  was  turbid  and  its  agglutinative  power  was  ten  times 

1  Osier  and  McCrae's  Mod.  Med.,  1913,  1,  123. 


ACUTE  SEROFIBRINOUS  PLEURITIS  ill 

that  of  the  patient's  blood  serum.  In  Gordinier  and  Lartigau's  case 
the  fluid  was  greenish-yellow  and  opalescent.  Pleural  effusions  in 
the  course  of  typhoid  fever  may  also  be  hemorrhagic,  but  arc  most 
commonly  purulent.  The  complication  may  occur  early,  as  in  Fernet' s 
case,  but  is  more  often  found  during  the  course  of  the  disease.  It  is 
not  certain  that  the  typhoid  bacillus  alone  is  capable  of  causing 
serofibrinous  effusion.  General  infection  with  typhoid  bacilli  is  so 
common  in  typhoid  fever  that  the  mere  presence  of  typhoid  bacilli 
in  the  exudate  does  not  suffice  to  establish  the  independence  of  typhoid 
pleuritis.  The  agency  of  other  organisms,  and  especially  the  tubercle 
bacillus,  must  be  rigorously  excluded.  In  Achard's  case  20  c.c.  failed 
to  produce  tuberculosis  in  an  inoculated  animal. 

(e)  Infection  in  any  part  of  the  body  may  be  a  cause  of  serofibrinous 
pleuritis,  although  the  effusion  accompanying  septic  processes  is  more 
often  purulent  in  character  or  becomes  so  after  passing  through  a 
serofibrinous  stage.  Pulmonary  infection  resulting  in  bronchopneu- 
monia, pulmonary  infarction,  pericarditis,  malignant  endocarditis, 
uterine  sepsis,  etc.,  may  lead  to  serofibrinous  pleuritis.  In  such  cases 
the  serous  rather  than  the  purulent  character  of  the  effusion  may  be 
due  to  the  small  number  or  diminished  virulence  of  the  infecting 
organisms  or  to  increased  resistance  on  the  part  of  the  patient. 

3.  Other  Causes. — A  sharp,  dividing  line  cannot  always  be  drawn 
between  transudates  and  exudates.  The  presence  of  fibrinous  flocculi 
or  clot  justifies  an  inclusion  in  the  class  of  serofibrinous  fluids.  Fibri- 
nogen is  present  in  all  fluids  and  an  admixture  with  blood  may  cause 
clotting.  An  inflammatory  process  may  readily  be  superadded  to  a 
transudate  and  thus  complicate  the  differentiation. 

Pathology.— 1.  Pleura. — The  appearance  of  the  pleura  does  not 
usually  differ  from  that  in  simple  fibrinous  pleuritis.  The  fluid  com- 
monly occupies  the  most  inferior  parts  of  the  cavity,  and  in  acute 
cases  the  fibrinous  layers  on  the  two  pleurae  are  usually  easily  separated 
where  they  lie  together  above  the  fluid.  Bands  of  adhesions  may 
traverse  the  fluid  and  connect  the  visceral  and  parietal  layers.  In 
the  more  chronic  cases  the  two  pleurae  may  be  more  or  less  firmly 
united  above  the  fluid.  It  is  less  common  to  observe  encapsulation 
of  serofibrinous  than  of  purulent  fluid.  Sacculated  exudates  are  most 
common  at  the  posterior  and  inferior  aspect  of  the  pleural  sac.  Rarely 
more  than  one  encapsulation  occurs,  and  the  contents  of  the  two  may 
vary,  in  one  serous,  in  the  other  purulent  fluid.  Miliary  tubercles 
may  occur  in  the  pleura  without  fluid  or  fibrinous  exudate.  Both 
fluid  and  fibrinous  exudate,  however,  are  more  common.  In  the  gross 
appearance  the  pleura  may  not  differ  from  that  seen  in  the  simple 
form,  and  tubercles  may  be  discovered  only  on  miscroscopic  examina- 
tion. 

2.  Side  Affected. — The  left  side  is  the  more  frequent  site  of  the 
process.  Of  1085  clinical  cases  the  effusion  was  confined  to  the  left 
side  in  570,  to  the  right  in  487,  while  both  were  involved  in  28.    In 


472  DISEASES  OF   THE  PLEURA 

one  the  effusion  was  sacculated  on  the  left,  posteriorly,  near  the  spinal 
column,  over  an  area  eight  inches  in  diameter. 

3.  The  Effusion. — This  is  quite  variable  in  its  character.  It  may  be 
largely  serous,  with  only  a  small  amount  of  scattered  fibrinous  flocculi. 
The  fibrin  may  exist  as  wavy,  skein-like  masses  in  suspension,  or  as 
more  compact,  whitish,  coarse,  membranous  shreds  or  curd-like 
deposits.  A  clot  usually  forms  in  a  variable  but  short  period  after 
evacuation,  and  may  be  found  as  a  small,  jelly-like  mass  at  the 
bottom,  or  may  comprise  almost  the  whole  volume  of  the  fluid,  with 
only  a  thin  layer  of  clear  serum  about  it.  The  fluid  is  usually 
amber  colored,  with  an  admixture  of  greenish  or  reddish  from 
the  presence  of  blood.  It  may  be  brownish  on  removal  or  turn 
so  after  standing.  When  mixed  with  considerable  amounts  of  blood 
it  may  be  blood  red,  and,  if  removed  after  having  long  remained  in 
the  chest,  may  be  darker,  even  chocolate  colored.  With  jaundice 
the  fluid  is  more  deeply  colored  and  responds  to  the  tests  for  biliary 
substances.  Most  fluids  are  clear  or  only  slightly  opalescent  from  the 
presence  of  albumin  in  fine  subdivision,  fibrin  in  the  form  of  flocculi, 
clot,  fat,  or  cellular  elements.  No  sharp  dividing  line  can  be  drawn 
between  serofibrinous  fluids  cloudy  from  the  presence  of  numerous 
cells  and  those  with  more  or  less  frank  admixture  of  pus.  It  must 
be  remembered  that  cellular  elements  tend  to  sediment  within  as  well 
as  outside  the  chest,  and  that  an  abundance  of  polynuclear  cells 
obtained  on  tapping  the  upper  layers  of  a  pleural  fluid  may  be  asso- 
ciated with  a  sediment  of  pus  at  the  bottom. 

(a)  The  amount  of  fluid  is  very  variable.  In  acute  fibrinous  pleuritis 
there  is  practically  always  more  than  the  normal  amount  of  fluid 
in  the  pleural  sac.  Even  when  the  process  is  confined  to  the  upper 
parts  of  the  pleura,  small  amounts  are  often  found  at  the  bases.  In 
500  cases  the  amount  varied  from  a  few  to  4620  c.c,  the  largest 
measured  amount  at  any  one  tapping.  The  right  chest  is  more  capa- 
cious than  the  left  and  larger  amounts  are  likely  to  be  present  in 
men  than  in  women. 

(b)  The  Reaction. — This  varies  with  phenolphthalein  and  litmus. 
Both  exudates  and  transudates  are  acid  to  phenolphthalein,  with 
inconstant  differences  in  the  degree  of  acidity.  "  Litmus  usually  reacts 
acid  to  exudates;  acid,  neutral  or  even  alkaline  to  transudates,  this 
apparent  discrepancy  being  due  to  the  disodium  phosphate,  which 
reacts  neutral  to  litmus  and  acid  to  phenolphthalein"  (Miller). 

(c)  Specific  Gravity. — The  determination  of  this  is  of  great  value  in 
differentiating  exudates  from  transudates.  The  fluid  should,  if  neces- 
sary, stand  several  hours  to  allow  the  escape  of  air  (Miller).  It  is 
surprising  with  what  constancy  inflammatory  fluids  have  a  specific 
gravity  of  1018  or  over.  Exceptions  are  not  common  even  in  a  large 
number  of  cases.  Of  224  cases  only  19  had  a  specific  gravity  below 
1018.  There  appears  to  be  no  noteworthy  difference  in  the  specific 
gravity  of  serofibrinous  fluids  accompanying  primary  disease  of  the 


ACUTE  SEROFIBRINOUS  PLEURITIS  473 

pleura,  those  associated  with  pulmonary  tuberculosis,  pneumonia, 
rheumatism,  typhoid  fever,  or  other  inflammatory  processes.  In 
transudates,  uncomplicated  by  inflammation  of  the  pleura,  the  specific 
gravity  is  usually  below  1018.  It  has  been  shown  that  the  amount 
of  salts  and  extractives  is  very  nearly  the  same  (Runeberg,  Mehu, 
Reuss,  Hoffman)  in  fluids  of  different  origin  and  after  the  removal  of 
albumin,  amount  to  about  1.08  per  cent,  in  non-inflammatory  fluids 
and  to  about  1.18  per  cent,  in  inflammatory  fluids.  A  variation  in 
the  specific  gravity  of  pleural  fluids  is  dependent  for  the  most  part 
on  differences  in  the  amount  of  albumin. 

(d)  Albumin. — This  exists  in  the  form  of  serum  albumin,  serum 
globulin,  and  fibrinogen,  to  which,  if  present  in  sufficient  amount,  is 
due  the  property  of  spontaneous  coagulation.  Inflammatory  fluids 
contain  a  relatively  large  amount  of  albumin  and  fibrinogen.  In 
general,  exudates  have  a  specific  gravity  of  1018  or  higher,  with  4 
per  cent,  or  more  of  albumin. 

Nucleo-albumin  (Primavera  and  Rivalta)  may  be  demonstrated  by 
the  addition  of  a  drop  of  the  fluid  to  be  tested  to  a  dilute  solution  of 
acetic  acid  (2  drops  glacial  acetic  to  200  c.c.  water).  If  nucleo-albumin 
is  present,  a  slight  turbidity  is  produced  in  the  fluid.  Runeberg  per- 
forms the  test  by  adding  a  few  drops  of  acetic  acid  to  the  fluid  to  be 
tested.  The  substance,  the  identity  of  which  is  uncertain,  is  demon- 
strated by  marked  turbidity  of  the  fluid  in  exudates  and  very  slight 
or  no  change  in  transudates.  It  is  somewhat  soluble  in  an  excess 
of  acetic  acid  and  completely  soluble  in  alkalies. 

The  determination  of  the  amount  of  albumin  in  these  fluids  is  of 
some  importance  in  judging  their  origin.  Estimation  by  weight  of 
the  precipitated  proteid  or  the  total  nitrogen  (Kjeldahl)  is  too  com- 
plicated for  general  use.  Esbach's  and  Purdy's  methods  of  estimating 
albumin  in  urine  are  only  approximately  accurate  for  pleural  fluids, 
as  is  shown  by  comparison  with  the  results  obtained  by  more  exact 
methods.  Reuss  has  devised  a  formula  for  estimating  the  amount 
of  albumin,  based  on  the  practical  lack  of  variation  in  salts  and  extrac- 
tives and  the  almost  constant  relation  between  the  specific  gravity 
and  albumin.  By  his  formula  A  =  f  (S  — 1000)  —  2.8,  in  which  A  = 
albumin  and  S  =  specific .  gravity,  the  amount  of  albumin  may  be 
calculated  and  the  error  amounted  to  as  high  as  0.5  per  cent,  in  only 
1  of  24  cases  in  which  the  albumin  was  carefully  determined  by  weight. 

(e)  Fat,  uric  acid,  cholesterin,  glucose,  biliary  acids,  and  pigments 
are  occasionally  found. 

(/)  Cellular  Elements. — The  sediment  obtained  after  standing 
or  sedimentation  shows  red-blood  corpuscles,  polynuclear  leukocytes, 
small  mononuclear  (lymphocytes)  and  endothelial  cells.  Eosinophiles 
and  mononuclear  cells  intermediate  between  the  small  lymphocyte 
and  endothelial  cell  are  common,  but  usually  comprise  only  a  small 
proportion  of  the  total  number.  An  occasional  mast-cell  is  not  an 
infrequent  finding. 


474  DISEASES  OF  THE  PLEURA 

Tuberculous  Fluids. — During  the  first  few  days  following  tuber- 
culous infection  of  the  pleura  there  may  be  an  excess  of  polynuclear 
cells,  as  lias  been  shown  by  Widal,  Tulland,  Wolff,  and  others,  but 
it  is  generally  agreed  that  fluids  i\\w  to  tuberculous  pleuritis  show  an 

excess  of  lymphocytes.  In  28  cases  (M.  G.  II.),  proved  to  be  tuber- 
culous by  the  finding  of  tubercle  bacilli  in  the  exudate  or  positive 
inoculation,  the  lymphocytes  numbered  90  to  100  per  cent,  in  24; 
88  per  cent,  in  1;  and  from  70  to  75  per  cent,  in  the  remaining  3,  of 
which  2  showed  15  per  cent,  endothelial  cells,  the  third  16  per  cent. 
eosinophiles.    The  lymphocytes  thus  predominated  in  all. 

In  effusions  arising  in  the  course  of  pulmonary  tuberculosis,  the 
lymphocytes  have  likewise  been  shown  to  predominate,  but,  owing 
to  the  chance  of  mixed  infection  from  the  lung,  a  variable  and  at 
times  considerable  proportion  of  polynuclear  cells  may  be  present. 
Of  19  cases  examined  by  Miller,  the  lymphocytes  comprised  95  per 
cent.,  or  more,  in  16.  Neutrophiles  predominated  in  1.  In  28  cases 
with  probable  or  certain  pulmonary  tuberculosis  (M.  G.  H.)  the  lym- 
phocytes numbered  80  to  100  per  cent,  in  20.  In  6  the  leukocytes 
were  degenerated,  in  1  there  were  about  equal  proportions  of  poly- 
nuclear cells,  while  in  the  last  case  the  endothelial  cells  numbered  85 
per  cent. 

Idiopathic  effusions  likewise  show  a  predominance  of  lymphocytes, 
and  for  this  as  well  as  other  reasons  should  be  mentioned  in  this  group. 
In  100  cases  (M.  G.  H.)  the  lymphocytes  ranged  from  70  to  100  per 
cent,  in  85.  In  14  of  the  remaining  cases  polynuclear  cells  were  in 
excess,  in  explanation  of  wrhich  a  mixed  infection  may  be  suspected. 
Small  endothelial  cells  reached  15  per  cent,  in  2,  in  1  case  numbering 
65  per  cent. 

Unfortunately,  not  all  fluids  showing  a  predominance  of  lymphocytes 
can  be  regarded  as  tuberculous  from  the  cellular  formula  alone.  Miller 
had  one  case  of  unknown  origin  with  97  per  cent,  lymphocytes  and  no 
reaction  to  tuberculin.  In  2  cases  (M.  G.  H.)  of  idiopathic  effusion, 
with  counts  of  over  95  per  cent,  of  lymphocytes,  there  was  no  reaction 
to  tuberculin.  Naunyn  has  observed  that  long-standing  transudates 
may  show  an  excess  of  lymphocytes,  and  this  is  confirmed  by  one  of 
the  present  series  with  95  per  cent,  lymphocytes  in  a  fluid  later  shown 
by  autopsy  (M.  G.  H.)  to  be  due  to  chronic  passive  congestion  and 
not  to  tuberculosis.  Despite  the  exceptions,  however,  a  predominance 
of  lymphocytes  must  be  regarded  as  strongly  suggestive  of  tuberculous 
pleuritis,  especially  when  passive  congestion  can  be  excluded. 

Infectious  {non-tuberculous)  Fluids. — Infection  of  the  pleura  with 
other  organisms  than  the  tubercle  bacillus  usually  gives  rise  to  an 
excess  of  polynuclear  cells  in  the  exudate.  Musgrave  studied  12 
cases;  the  polynuclear  cells  predominated  in  all.  Miller  reported  7 
cases.  The  neutrophiles  were  in  excess  in  most,  but  in  2,  one  of  whom 
failed  to  react  to  tuberculin,  there  were  97  per  cent,  of  lymphocytes. 
In  my  series  there  are  counts  on  16  cases.    In  general,  the  fluids  differed 


ACUTE  SEROFIBRINOUS  PLEURtTIS  475 

from  those  obtained  in  tuberculous  cases  in  their  more  turbid  character, 
the  lower  percentage  of  lymphocytes  and  higher  proportion  of  poly- 
nuclear  and  endothelial  cells.  In  1  of  11  metapneumonic  effusions 
the  lymphocytes  numbered  82  per  cent.  In  2  cases  associated  with 
an  arthritis,  there  were  65  and  95  per  cent,  polynuclears.  The  lymph- 
ocytes predominated  in  2  of  3  cases  in  which  the  effusion  followed 
trauma.  Tuberculosis  could  not  be  excluded.  Naunyn  states  that 
lymphocytes  may  predominate  in  acute  cases  which  are  subsiding, 
or  in  mild  infections. 

For  transudates,  endothelial  cells  in  large  numbers  occurring  espe- 
cially in  sheets  or  plaques,  are  characteristic,  but  lymphocytes  may 
predominate  in  mechanical  effusions  of  long  standing.  A  secondary 
infection  may  modify  the  cellular  formula,  with  relative  increase  in 
polynuclear  cells. 

The  value  of  cytology  in  the  diagnosis  of  the  cause  of  pleural  effusions 
has  proved  somewhat  less  valuable  than  was  at  first  anticipated.  The 
exceptions  are  too  numerous  to  admit  of  definite  conclusions  from  the 
cells  alone,  but  the  method  is  of  assistance  with  other  factors  in  any 
given  case. 

4.  Intrapleural  Tension. — With  small  effusions  this  may  still  be 
negative.  As  the  fluid  increases  in  amount  the  tension  rises  and 
becomes  positive  after  the  pulmonary  elasticity  is  spent.  Various 
factors  influence  the  pressure.  It  may  be  relatively  high  with  a  small 
amount  of  fluid  if  pulmonary  retraction  is  prevented  by  pleural 
adhesions,  by  pulmonary  or  mediastinal  disease.  Pitres1  finds  that 
the  pressure  may  vary  from  0  to  +2  or  +3  with  less  than  1000  c.c, 
from  +8  to  +22  with  1000  to  2000  c.c,  and  from  +20  to  +48  mm. 
Hg.  with  more  than  2000  c.c.  The  pressure  fluctuates  with  the  phases 
of  respiration.  An  initial  positive  pressure  may  fall  during  deep 
inspiration  to  —  40,  as  noted  by  Schreiber.2  After  aspiration  the  fall 
may  be  greater  and  with  deep  inspiration  even  to  —90  mm.  Hg.  The 
fluid  is  also  under  a  pressure  of  its  own  fluid  column  and  the  tension 
thus  varies  at  different  levels. 

5.  Mechanical  Effects  of  the  Exudate. — With  small  effusions  the  lung 
contracts  and  becomes  atelectatic.  With  large  effusions  it  is  com- 
pressed, completely  emptied  of  air,  and  for  the  most  part  of  blood, 
and  may  be  found  as  a  brown  mass,  not  larger  than  the  closed  fist, 
lying  against  the  spinal  column  in  the  upper  and  posterior  part  of 
the  affected  side.  In  the  absence  of  long-standing  and  extensive 
inflammatory  changes  it  is  still  capable  of  reexpansion  after  removal 
of  the  fluid.  Under  less  favorable  circumstances,  extensive  adhesions, 
the  formation  of  dense  connective  tissue  on  its  surface  and  within 
its  substance  may  prevent  this.  Such  a  result  is  much  less  common 
with  serofibrinous  than  with  purulent  exudates,  and  since  it  has 
become  the  custom  to  tap  early.      The  belief  is  held  by  some  that 

1  Arch.  clin.  de  Bordeaux,  1896,  v,  70.  2  Deut.  Arch.  f.  klin.  Med.,  vol.  xxxiii. 


476  DISEASES  OF  THE  PLEURA 

persistent  effusions  exert  a  favorable  effect  on  tuberculous  processes 
in  the  neighboring  lungs  in  consequence  of  mechanical  compression 
and  immobilization,  but  this  is  doubtful,  and  the  danger  of  secondary 

changes  in  the  pleura  and  lung  offset  any  fancied  advantage  in  allow- 
ing the  fluid  to  remain. 

In  consequence  of  diminished  negative  pressure  within  the  thorax, 
the  intercostal  spaces  show  less  than  their  normal  depression.  Early 
in  the  disease  they  may  be  narrowed  from  spasm  of  the  intercostal 
muscles.  With  large  effusion  and  increase  in  size  of  the  affected  side 
the  spaces  may  actually  be  widened  from  pressure,  and  perhaps, 
also,  from  paralysis  of  the  intercostals.  Later,  following  the  absorp- 
tion or  removal  of  fluid,  the  thoracic  wall  may  be  depressed,  and  the 
intercostal  spaces  narrowed  from  contraction  of  scar  tissue.  The 
diaphragm,  and  with  it  the  liver  or  spleen,  is  at  first  depressed  from 
the  loss  of  the  normal  negative  intrathoracic  pressure.  With  large 
effusions,  the  diaphragm  is  forced  downward  by  positive  pressure  from 
above  and  the  weight  of  the  superimposed  fluid.  The  dislocation  of 
the  mediastinum  and  the  heart  from  small  effusions  is  a  result  of  a 
disturbance  of  equilibrium  between  the  two  pleural  sacs.  It  is  dis- 
located by  positive  pressure  writh  large  effusions.  Pressure  on  the 
esophagus  may  lead  to  dysphagia,  and  pressure  on  or  invasion  of  the 
region  about  the  vagus,  to  recurrent  laryngeal  paralysis. 

The  ultimate  causes  of  circulatory  symptoms  have  been  the  subject 
of  much  experimentation.  They  do  not  appear  to  be  due  to  changes 
in  the  blood-pressure  from  narrowing  of  the  pulmonary  circulation, 
which  may  be  obstructed  even  to  four-fifths  of  its  extent  without  a 
permanent  fall  of  blood  pressure  (Lichtheim  et  al.).  Even  a  slight 
increase  of  intrathoracic  pressure,  however,  leads  to  considerable 
circulatory  disturbance,  as  is  seen  in  the  swelling  of  the  cervical  veins 
in  coughing  and  straining.  I).  Gerhardt1  believes  this  to  be  due  to 
diminished  outflow  of  blood  from  the  intrathoracic  veins,  obstruction 
to  the  pulmonary  capillaries  and  veins,  and  reflex  depressor  action. 
Compensation  may  be  effected  by  increased  depth  of  respiration. 
Toxins,  fever,  carbon  dioxide  poisoning,  or  existing  cardiac  disease 
may  likewise  be  factors. 

6.  Protective  Action  (?)  of  the  Effusion. — Aside  from  the  favorable 
action  which  an  effusion  may  be  thought  to  possess  in  the  limitation 
of  motion  of  the  affected  lung,  a  conservative  function  has  been 
assumed  on  the  ground  that  it  may  contain  protective  substances. 
At  present  this  can  neither  be  denied  nor  affirmed.  Opie's  studies2 
on  pleurisy  induced  in  dogs  by  intrapleural  injection  of  turpentine 
may  have  a  bearing  on  this  question.  He  finds  that  the  fibrinous 
exudate  contains  a  proteolytic  enzyme  (or  enzymes)  the  exuded 
serum  an  anti-enzyme,  which  prevents  autolysis  and  promotes  resolu- 
tion.   In  his  experiments  removal  of  fluid  appeared  to  hasten  autolysis, 

1  Zeit.  f.  klin.  Med.,  1904,  vol.  lv.  2  Trans.  Assoc.  Amer.  Phys.,  1907,  vol.  xxii. 


ACUTE  SEROFIBRINOUS  PLEURITIS  477 

and  promote  incomplete  resolution  and  greater  abundance  of  fibrin. 
It  may  even  induce  empyema  in  dogs.  The  danger  of  transforming  a 
serofibrinous  effusion  into  empyema  by  the  withdrawal  of  fluid,  as 
suggested  by  Opie's  experiments,  appears  to  be  insignificant  in  clinical 
cases. 

7.  Absorption. — Various  factors  probably  play  a  part  in  absorption. 
Hydremic  and  congestive  transudates  are  rapidly  absorbed  under 
favorable  conditions.  Inflammatory  fluids  containing  relatively  few 
formed  elements  and  fibrin  may  likewise  spontaneously  disappear. 
Purulent  fluids,  however,  may  remain  indefinitely  unless  evacuated 
by  perforation  or  operation.  Large  effusions  are  less  often  absorbed. 
The  mechanism  is  probably  largely  mechanical.  Small,  serous, 
effusions,  unassociated  with  fibrinous  obstruction  of  pleural  lymphatics, 
and  interfering  relatively  little  with  respiratory  changes  of  intrapleural 
pressure,  are  most  favorable  for  absorption,  while  the  opposite  obtains 
in  large  and  inflammatory  fluids.  West1  refers  to  the  "  lymphatic- 
pump,  "  the  action  of  which  is  suspended  by  fibrin  plugging  the  pleural 
stomata  and  large  effusions  which  prevent  aspiration  on  the  affected 
side.  It  is  probable  that  osmosis,  also,  is  a  factor.  Rothschild2  finds 
that  fluids  showing  less  molecular  concentration  than  the  blood,  as 
indicated  by  a  higher  freezing  point,  are  more  likely  to  be  absorbed 
than  those  in  which  the  opposite  relation  obtains.  In  the  latter 
instance  abstraction  of  fluid  from  the  blood  may  increase  the  amount 
of  pleural  fluid  until  isotonicity  is  established.  Absorption  is  delayed 
by  the  production  of  artificial  pneumothorax  as  shown  by  Fleiher3 
and  Naegeli.4 

Symptoms  — 1.  Primary  Form. — Prodromata  are  uncommon.  Slight 
cough  and  failing  health  may  precede  the  onset.  An  initial  chill 
is  rare;  chilliness  is  common.  The  disease  began  gradually  in  more 
than  one-half  (60  per  cent.)  of  my  series.  There  is  malaise,  pain 
of  variable  intensity,  fever,  and  cough.  Sudden  onset,  in  which  the 
patient's  activity  is  abruptly  interrupted,  is  less  common.  In  excep- 
tional cases  the  initial  features  may  suggest  pneumonia.  There  is 
chill,  fever,  and  severe  pain  in  the  side,  but  no  rusty  sputum.  An 
insidious  onset,  especially  at  the  extremes  of  age,  is  not  infrequent. 
In  a  small  proportion  the  symptoms  are  sufficiently  characteristic 
to  suggest  the  diagnosis  from  the  history  of  initial  pain,  which  gradu- 
ally diminishes  or  stops  as  the  fluid  accumulates  and  the  dyspnea 
increases.  The  temperature  may  gradually  rise  as  long  as  the  fluid 
increases,  is  continuous  during  this  period,  intermittent  with  the  effu- 
sion at  a  standstill,  and  often  absent  during  absorption.  It  may  reach 
normal  at  the  end  of  a  week  or  ten  days,  although  continuous  or 
irregular  fever  may  last  for  a  much  longer  period.  The  exudate  may 
be  discovered  by  the  third  or  fourth  day;  if  untapped,  may  gradually 

1  Lancet,  March  25,  1905.  2  Deutsch.  Aerzteztg.,  1901,  H.  40,  p.  241. 

3  Virchow's  Arch.,  vol.  cxii,  pp.  97  and  282. 

4  Zeit.  f.  d.  gesamte  exp.  Med.,  12  Marz,  1913. 


178  DISEASES  OF   THE  PLEURA 

increase  during  the  next  ten  days,  then  gradually  diminish,  to  disap- 
pear in  favorable  cases  during  the  third,  fourth,  or  fifth  week  of  the 
illness. 

The  disease  is  often  atypical.  General  symptoms  and  fever  may 
predominate,  and,  aside  from  the  pulmonary  findings,  typhoid  fever 
may  be  suggested.  Pain  in  the  abdomen,  with  muscular  spasm  and 
tenderness,  may  mislead  the  observer  into  the  diagnosis  of  an  acute 
abdominal  affection.  Both  onset  and  course  may  be  latent  or  sudden, 
severe,  even  rapidly  fatal  (pleuritis  acutissima).  There  may  be  an 
initial  chill,  rapid  rise  of  temperature,  intense  dyspnea,  cyanosis, 
rapid  pulse  and  respiration,  delirium,  and  death  in  a  few  days  with 
symptoms  of  suffocation.  An  immediate  resort  to  evacuation  may 
be  life  saving  in  such  cases. 

2.  Secondary  Form. — The  onset  and  course  are  often  so  masked  by 
the  existing  disease  that  symptoms  referable  to  the  pleura  are  unnoticed 
or  absent.  The  presence  of  pleural  effusion  may  then  be  discovered 
only  during  a  routine  physical  examination,  or,  if  this  is  neglected 
and  the  disease  is  fatal,  at  autopsy.  The  presence  or  absence  of  symp- 
toms largely  depends  on  the  mildness  or  severity  of  the  primary 
disease.  In  pulmonary  tuberculosis,  however,  the  symptoms  may  be 
typical,  since  effusion  usually  occurs  early,  if  at  all,  in  its  course, 
from  the  frequent  obliteration  of  the  pleural  sac  by  adhesions  in  the 
more  advanced  stages.  In  lobar  pneumonia,  typical  symptoms  of 
effusion  are  usually  lacking  or  only  with  difficulty  differentiated  from 
those  due  to  the  pneumonia  itself.  There  may  be  an  accession  of 
pain,  dyspnea,  or  cough.  The  respirations,  pulse,  and  temperature 
may  rise  above  their  previous  level.  A  failure  of  the  temperature 
to  drop  at  the  expected  time  may  be  the  first  indication. 

3.  Special  Symptoms. — Pain. — This  is  usually  one  of  the  first  and 
most  typical  symptoms.  It  was  present  in  89  of  100  cases  of  primary 
serofibrinous  effusion  in  this  series.  It  may  be  absent,  as  in  5  cases. 
Associated  tenderness  over  the  inflamed  pleura  is  frequent. 

Cough.— This  is  probably  next  in  frequency,  occurring  in  83  per 
cent.,  absent  in  12  per  cent.,  and  not  given  in  5  per  cent.  It  is  usually 
short  and  dry,  but  may  be  accompanied  by  expectoration  (48  per 
cent.).  The  sputum  is  mucoid  or  muco-purulent;  rarely  it  may  con- 
tain blood  (2  per  cent.)  Cough  alone  may  be  due  to  pleural  irritation. 
Expectoration  should  suggest  a  pulmonary  complication,  usually  an 
infection,  more  rarely  edema,  evidence  of  which  may  be  furnished  by 
the  character  of  the  sputum. 

Respiration. — Short,  quick  respiration  is  frequent  in  the  early  stages 
from  pain  and  spasm  of  the  respiratory  muscles.  The  rate  may  be 
elevated  from  fever,  encroachment  on  the  thoracic  space  by  fluid, 
associated  pulmonary  disease,  or  embarrassment  of  the  circulation 
from  pressure.  The  normal  relation  between  the  rate  of  respiration 
and  pulse  is  much  more  often  maintained  with  pleural  effusion  than 
with  pneumonia.     Quick  respiration  is  more  often  observed  at  the 


ACUTE  SEROFIBRINOUS  PLEURITIS  479 

onset  and  after  exertion.  When  the  patient  is  at  rest  and  the  exudate 
has  gradually  accumulated,  one  side  of  the  chest  may  contain  its  full 
capacity  of  fluid  without  disturbance  of  the  normal  respiration-pulse 
ratio. 

Dyspnea. — The  embarrassment  of  respiration  may  amount  to 
dyspnea.  This  is  more  frequent  in  rapidly  formed  and  large  accumu- 
lations, and  may  become  orthopnea.  At  times,  however,  with  small 
effusions  and  much  limitation  of  respiratory  motion,  there  may  be 
marked  dyspnea.  Cyanosis,  with  or  without  turgescence  of  the 
cervical  veins,  is  likely  to  accompany  marked  interference  with  res- 
piration. 

Temperature. — There  is  no  typical  fever  curve.  The  temperature 
is  more  often  elevated  and  in  general  reaches  a  higher  level  than 
with  dry  pleurisy.  Of  100  primary  cases  in  my  series,  only  10  were 
without  fever.  From  100°  to  102°  is  an  average  pyrexia.  In  rare  in- 
stances the  temperature  may  reach  104°  to  105°  or  higher.  It  is  likely 
to  be  high  in  children  and  robust  patients.  Absence  of  fever  is  occa- 
sionally observed  in  old  or  debilitated  patients  and  in  terminal  infec- 
tions, when  it  may  be  subnormal. 

Pulse. — This  presents  no  special  features.  The  rate  usually  corres- 
ponds to  the  fever  curve.  The  rapid  accumulation  of  a  large  amount 
of  fluid  may  embarrass  the  circulation  and  cause  a  rapid  and  feeble 
pulse. 

Febrile  or  Toxic  Symptoms. — These  are  not  especially  characteristic 
and  are  such  as  may  be  seen  in  other  infectious  processes.  At  the  onset 
there  may  be  headache,  insomnia,  malaise,  and  general  pains.  The 
skin  is  hot  and  dry.  As  the  fever  drops,  there  may  be  sweating,  which 
may  become  a  prominent  symptom  if  the  process  is  long  continued. 
There  may  be  thirst,  anorexia,  even  nausea  and  vomiting,  but  gastric" 
disturbances  are  uncommon.  In  protracted  cases  the  loss  of  strength 
and  weight  may  be  marked. 

Hoarseness  may  be  due  to  pressure  on  or  paralysis  of  the  recurrent 
laryngeal  nerve.  Dysphagia  from  pressure  on  the  esophagus  may  be 
present.  Ferber  has  observed  that  the  passage  of  food  through  the 
esophageal  foramen  may  be  accompanied  by  pain,  when  there  is 
diaphragmatic  pleurisy.  Singultus  is  a  rare  and  interesting  symptom. 
It  may  be  most  distressing  when  the  diaphragm  is  involved. 

Urine. — During  the  acute  stage,  the  urine  presents  the  usual  features 
common  to  febrile  disturbances.  It  is  small  in  amount,  of  high  color 
and  specific  gravity,  with  an  increase  of  urea  and  uric  acid  and  a 
diminution  in  the  chlorides.  During  absorption,  the  amount  may 
rise  rapidly  with  an  increase  in  the  output  of  chlorides,  the  so-called 
"chlorine  crisis,"  while  urea  and  uric  acid  are  diminished.  Traces  of 
albumin  and  a  few  hyaline  casts  may  be  present  and  can  be  ascribed 
to  fever,  toxemia,  or  rarely  to  statis. 

Physical  Signs. — Small  amounts  of  fluid  collect  in  the  most  depen- 
dent part  of  the  thoracic  cavity,  in  the  costophrenic  sinus  posteriorly, 


180  DISEASES  OF   THE   PLEURA 

and  in  the  region  between  lung  and  diaphragm.  Until  the  amount 
of  fluid  becomes  considerable,  it  intervenes  very  little  between  lung 
and  chest  wall.  In  Garland's  experiments  there  was  scarcely  a  trace 
of  a  rim  of  fluid  between  the  lower  border  of  the  lung  and  the  chest 
wall,  with  injections  which  occupied  less  than  one-third  of  the 
thoracic  cavity.  In  explanation  of  this  it  is  assumed  that  there  is 
a  greater  clastic  traction  in  the  lower  than  in  the  upper  parts  of  the 
lung.  Larger  amounts  finally  intervene  between  lung  and  chest  wall. 
In  favorable  and  uncomplicated  cases,  250  c.c.  of  fluid  in  an  adult 
should  not  escape  detection.    In  infants  100  c.c.  may  be  discovered. 

Inspection. — Herpes  is  uncommon.  Inspiratory  dilatation  of  the 
alse  nasi  is  less  frequent  than  with  pneumonia.  The  position  of  the 
patient  is  variable.  If  there  is  dyspnea,  the  patient  may  be  more 
comfortable  sitting  upright,  from  the  greater  mechanical  advantage 
and  from  the  removal  6f  the  weight  of  the  effusion  on  the  lung  which 
this  position  affords.  With  small  effusions,  without  orthopnea,  the 
patient  may  be  more  comfortable  on  the  unaffected  side.  The  explana- 
tion of  this  is  not  clear.  It  may  be  due  to  the  relief  of  pain  from 
removal  of  pressure  on  sensitive  nerves  in  the  affected  pleura.  With 
large  effusions,  the  patient  usually  chooses  a  position  on  the  affected 
side,  thus  allowing  the  sound  lung  full  play  and  diminishing  pressure 
on  the  mediastinum.  It  is  not  uncommon,  even  with  large  effusions, 
to  find  the  patient  lying  comfortably  on  the  back.  x\t  times  an 
ambulant  patient  presents  himself  with  a  large  effusion. 

In  the  early  stages  of  the  disease,  when  there  is  pain  and  only  a  small 
amount  of  fluid,  the  appearance  of  the  thorax  does  not  differ  from  that 
described  under  Fibrinous  Pleuritis.  WTith  increase  in  the  amount 
of  pleural  fluid,  there  is  progressively  less  expansion  and  elevation  of 
the  affected  side.  The  presence  of  pain  always  still  further  limits 
thoracic  motion.  Diminished  motion  may  often  be  apparent  as  a 
delay  in  expansion  of  the  lowTer  parts  of  the  chest  during  the  first  part 
of  inspiration.  With  large  amounts  of  fluid,  expansion  and  elevation 
may  be  absent.  The  intercostal  spaces  in  spare  individuals  may  be 
seen  to  have  lost  their  normal  depression  and  may  even  be  widened 
and  fuller  than  normal.  An  increase  in  size  can  be  confirmed  by  the 
tape,  even  as  much  as  an  inch  or  an  inch  and  ,a  half  greater  than  the 
opposite  side.  The  skin  may  appear  somewhat  shiny  and  smooth 
from  obliteration  of  normal  furrows  and  depressions.  Edema  of  the 
skin  and  dilatation  of  the  superficial  veins  may  occur,  but  are  rare  with 
serous  effusion.  Weisz1  finds  that  the  phonation  phenomenon  (visible 
voice  vibrations)  is  transmitted  through  fluid  and  may  separate  its 
lower  .limit  from  the  upper  border  of  the  liver. 

In  consequence  of  the  fulness  of  the  affected  side,  the  distance 
between  the  median  line  and  the  nipple  in  front  and  the  scapula  behind 
may  exceed  that  on  the  normal  side.     With  large  effusions  the  cor- 

1  Prag.  med.  Woch.,  1905,  xxx,  261. 


ACUTE  SEROFIBRINOUS  PLEUB1TIS  481 

responding  hypochondrium  may  be  fuller.  The  shoulder  and  with  it 
the  outer  end  of  the  clavicle  stand  at  a  higher  level.  Following  partial 
or  complete  absorption  or  withdrawal  of  fluid,  the  affected  side  may 
be  somewhat  diminished  in  size  and  the  intercostal  spaces  narrowed. 
Slight  lateral  deviation  of  the  spine  may  accompany  this  retraction. 
Retraction  and  scoliosis  are  much  less  marked  after  serous  than  after 
purulent  fluids. 

The  diaphragm  shadow  is  absent  on  the  side  of  the  effusion.  It 
usually  remains  absent  after  recovery,  but  may  return,  although 
practically  always  of  diminished  amplitude.  The  position  of  the 
cardiac  impulse  should  be  inspected.  Evidence  of  pleuropericardial 
adhesions  may  be  obtained  by  systolic  depression  of  the  intercostal 
spaces  in  an  abnormal  position  in  the  cardiac  region. 

Rarely  ■pulsation  of  the  chest  wall  may  be  observed  with  serofibrinous 
effusion,  but  is  more  common  with  pus.  The  pulsation  may  be  con- 
fined to  a  locally  bulging  area;  it  may  be  circumscribed  without  tumor 
or  may  be  diffuse.  Instances  have  been  reported,  among  others,  by 
Cruveilhier,  Flint,  Broadbent,  and  Osier.  Cases  of  pulsating  hemo- 
thorax have  been  observed  by  Vialle  and  Braun,  Montegre,  McPhedran, 
and  Sailer,1  who  gives  an  account  of  the  literature  to  1904.  In  Sailer's 
case  there  was  true  expansile  pulsation  of  the  whole  thorax. 

Palpation. — This  may  confirm  the  results  of  inspection.  A  differ- 
ence in  the  expansion  of  the  two  sides  of  the  chest,  the  condition  of  the 
intercostal  spaces,  the  degree  of  separation  of  the  ribs,  the  position  of 
the  cardiac  impulse  and  pulsations  in  other  parts  of  the  chest  may  be 
more  evident  to  the  hand  than  the  eye.  Pulsation,  indeed,  may  be 
so  slight  as  to  be  appreciated  only  by  the  hand.  A  narrowing  and  a 
more  marked  resistance  to  pressure  in  the  interspaces  may  occur  early 
in  the  disease  from  spasm  of  the  intercostals,  and  is  an  important  sign. 
The  interspaces  may  be  narrowed  even  when  the  affected  side  is  in- 
creased in  size.  A  friction  rub  may  be  felt  before  the  onset  of  effusion; 
it  may  be  palpated  outside  the  limits  of  fluid  during  the  course  of  the 
disease  and  may  return  following  absorption.  The  temperature  of 
the  affected  side  is  higher.  Edema  and  fluctuation  are  rare  with 
serous  effusion.  The  liver  or  spleen  may  be  displaced  downward. 
The  diaphragm  may  be  so  far  depressed  as  to  be  felt  below  the  costal 
margin. 

The  tactile  fremitus  is  practically  always  absent ;  it  is  rarely  present, 
but  usually  even  then  diminished,  in  children,  with  adhesions  between 
the  visceral  and  parietal  pleura,  or  with  small  effusions.  This  is  one 
of  the  most  important  signs  of  fluid.  The  dividing  line  between 
lung  and  fluid  can  often  be  sharply  drawn  at  the  level  at  which  the 
voice  vibrations  are  lost.  The  tactile  fremitus  above  the  fluid  may  be 
diminished,  maintained,  or  increased,  depending  on  the  condition  of 
the  pleura  and  the  lung.     Unfortunately,  fremitus  cannot  always  be 

1  Artier.  Jour.  Med.  Sci.,  1904. 
31 


482  DISEASES  OF   THE   PLEURA 

obtained  in  women  or  children,  owing  to  the  high  pitch  of  the  voice 
or  the-presence  of  an  abundant  layer  of  subcutaneous  fat.  Acute  or 
chronic  inflammatory  thickening  of  the  pleura  diminishes,  although 
it  practically  never  abolishes,  the  fremitus.     In  the  performance  of 

thoracentesis  a  localized  area  where  fremitus  is  maintained  should 
not  be  chosen,  because  of  the  possibility  of  pleural  adhesions  at  this 
place. 

Percussion. — Light  is  far  superior  to  heavy  percussion  in  bringing 
out  slight  changes  in  the  pleura.  Early  in  the  disease,  when  there  is 
only  a  small  amount  of  fluid,  no  change  in  the  percussion  note  may  be 
detected.  As  the  fluid  increases  there  is  dulness  at  the  base.  As  the 
fluid  rises,  the  note  becomes  less  resonant  and  finally  flat.  The  region 
of  flatness  and  absent  tactile  fremitus  correspond.  The  percussion 
note  over  effusions  of  considerable  size  is  of  short  duration,  lacking 
in  volume,  of  high  pitch,  very  nearly  like  the  note  obtained  on. per- 
cussing the  thigh.  It  is  very  difficult  to  mark  on  the  chest  the  exact 
upper  limit  of  fluid.  With  considerable  fluid,  three  zones  with  well- 
marked  differences  in  the  percussion  note  can  be  made  out  in  the 
anterior  and  more  often  in  the  posterior  thoracic  regions.  Normal 
or  diminished  vesicular  resonance  may  be  obtained  in  the  uppermost 
parts  of  the  chest.  Between  this  region  and  the  fluid  the  note  is  dull, 
but  has  a  tympanitic  quality  (Skoda's  resonance),  due  to  retraction 
or  compression  of  the  lung  and  vibration  of  air  in  the  bronchi  or  trachea. 
Below,  there  is  flatness  from  fluid.  The  intermediate  dull  or  dull  and 
tympanitic  area  is  usually  most  marked  behind,  in  the  interscapular 
region,  but  with  large  effusions  may  be  detected  in  front,  under  the 
clavicle.  If  an  arbitrary  distinction  be  made  between  resonance  and 
dulness  and  dulness  and  flatness,  a  triangular  area  of  dulness  or  dull 
tympany  can  be  marked  out  in  the  interscapular  region,  between  the 
relatively  normal  lung  above  and  the  fluid  below.  This  triangle  has 
for  its  base  the  vertebral  column,  for  its  lower  side  the  lower  limit 
of  lung,  corresponding  to  the  beginning  of  flatness,  for  its  upper  limit 
the  beginning  of  dulness.  The  triangle  represents  the  retracted  or 
compressed  lung,  which  may  be  apposed  to  the  chest  wall  in  this 
region.  Its  recognition  is  important  for  the  correct  determination 
of  the  upper  limit  of  the  effusion.  The  tympanitic  note  observed 
above  the  layer  of  fluid,  as  over  pulmonary  cavities,  may  change  in 
pitch  with  the  mouth  open  and  closed  (Williams'  tracheal  tone)  during 
inspiration  and  expiration  (Friedreich's  phenomenon),  and  on  chang- 
ing the  position  of  the  patient  (Gerhardt's  phenomenon).  A  cracked- 
pot  sound  also  may  be  heard  in  the  absence  of  cavity. 

With  right-sided  effusion,  the  dulness  merges  below  with  that  of 
the  liver.  On  the  left,  the  tympany  from  inflation  of  the  stomach 
with  gas  may  be  confusing  and  mask  slight  changes  in  the  note  from 
fluid.  With  considerable  fluid  in  the  left  pleura,  the  normal  tympany 
of  the  semilunar  space  between  liver  and  spleen  (Traube's  semilunar 
space)  mayjje  obliterated. 


ACUTE  SEROFIBRINOUS  PLEURIT1S  483 

Curved  Line  of  Flatness  in  Pleural  Effusions. — The  limitation  of 
fluid  by  dulness  by  some  observers,  and  flatness  by  others  is  respon- 
sible for  much  confusion  in  the  description  of  the  line  assumed  by  the 
upper  border  of  pleural  fluid.  If  the  dull  triangle  mentioned  above 
be  included,  the  upper  limit  of  fluid  is  nearly  horizontal  behind.  With 
a  small  or  medium  effusion,  however,  the  line  of  flatness  only  should 
be  regarded  as  indicating  its  upper  limit. 

Damoiseau  was  the  first  to  note  that  the  upper  limit  of  flatness  was 
a  curved  and  not  a  straight  line.  Ellis,  of  Boston,  correctly  traced 
the  curve,  which  Garland1  verified  clinically  and  explained  by  a  series 
of  experiments. 

For  the  demonstration  of  the  curve  the  patient  must  be  in  the 
upright  position.  It  is  best  indicated  by  light  percussion,  in  parallel 
lines,  perpendicular  to  the  upper  line  of  the  effusion,  which,  in  general, 
is  transverse  about  the  chest.  With  small  or  medium  effusions,  the 
general  shape  of  the  curve  is  that  of  an  elongated  "S,"  lowest  behind, 
advancing  upward  and  forward  to  the  axillary  region,  where  it  is 
highest,  thence  sloping  gradually  downward.  With  large  effusions 
the  curve  may  be  flattened  out  to  assume  a  more  nearly  horizontal 
line.  The  curves  of  the  line  of  flatness  correspond  to  the  line  of  apposi- 
tion between  the  lower  border  of  the  lung  and  the  pleural  fluid.  It 
is  thus  the  shape  of  the  lower  border  of  the  lung  which  gives  to  the 
line  the  shape  of  the  elongated  letter  "S."  The  elastic  retraction  of 
the  lung  supports  a  certain  volume  of  fluid  and  prevents  its  upper 
limit  from  assuming  a  hydrostatic  level. 

The  curve  may  be  of  diagnostic  value  as  a  confirmatory  sign  of 
pleural  effusion.  It  cannot  be  demonstrated  in  circumscribed  effusions, 
in  the  presence  of  adhesions,  or  in  other  than  the  upright  position. 
Pulmonary  infiltration,  by  diminishing  the  elasticity  of  the  lung,  may 
render  difficult  or  prevent  the  demonstration  of  the  curve.  It  makes 
no  difference  whether  the  fluid  be  serum  or  pus.  The  curve  is  more 
pronounced  with  fluids  undergoing  absorption  or  after  partial  removal 
by  tapping,  a  possible  explanation  for  which  may  be  the  presence 
of  pleural  adhesions  in  the  lateral  thoracic  region,  maintaining  the 
lung  at  a  higher  level  here,  while  posteriorly,  where  fluid  collects  in 
greater  amount,  its  intervention  between  lung  and  chest  wall  may 
prevent  the  formation  of  adhesions. 

Shifting  Dulness. — Dulness  due  to  pleural  effusion  shifts  on  changing 
the  position  of  the  patient.  This  is  especially  true  of  small  and  recent 
effusions.  With  the  patient  upright,  then  in  the  horizontal  position 
the  upper  border  of  fluid  changes  its  level.  It  is  absent  in  the  presence 
of  encapsulating  adhesions  and  may  be  slight  or  absent  with  large 
effusions.  Due  allowance  in  noting  shifting  dulness  must  be  made 
for  normal  changes  in  the  percussion  note  over  the  chest  in  different 
positions.    The  posterior  inferior  parts  of  the  lung,  where  the  test  is 

1  Boston  Med.  and  Surg.  Jour.,  September  17,  1874,  and  Pneumono-dynamics,  Boston, 

1878. 


1M  DISEASES  OF  THE  PLEURA 

usually  made,  normally  become  more  resonant  when  the  patient 
assumes  a  horizontal  position,  as  in  bending  forward  or  lying  face 
downward.  The  maintenance  of  one  position  during  the  development 
of  an  effusion  is  capable,  to  a  certain  extent,  of  modifying  the  location 
of  the  fluid.  If  the  patient  has  been  constantly  on  his  back,  the  upper 
limit  of  fluid  is  likely  to  be  higher  behind,  and  small  effusions  may  be 
confined  to  the  back  and  posterior  axilla.  It  should  be  remembered 
in  testing  shifting  dulness  that  the  fluid  may  change  its  position  only 
slowly. 

Sense  of  Resistance. — In  addition  to  the  lack  of  resonance  or  other 
peculiarities  of  the  percussion  note  appreciated  by  the  ear,  the  lack 
<  »f  vibration  and  sense  of  resistance  may  be  apparent  to  the  finger  as  well. 

Auscultation. — Early  in  the  disease,  a  friction  rub  may  be  heard. 
Its  presence  does  not  exclude  fluid,  which  may  exist  between  lung  and 
diaphragm  or  in  the  neighborhood  of  apposed  pleural  surfaces.  With 
small  effusions,  the  rub  not  infrequently  persists  in  the  lower  anterior 
or  lateral  portions  of  the  chest.  The  disappearance  of  this  sign  as 
fluid  accumulates  is  probably  due  not  so  much  to  intervention  of  fluid 
between  lung  and  chest  wall  as  to  the  mechanical  obstruction  to  the 
expansion  of  the  lung.  The  re-appearance  of  friction  in  cases  with 
pleural  effusion  is  favorable,  indicating  diminution  or  disappearance 
of  fluid,  provided  extension  of  fibrinous  pleuritis  to  previously  unin- 
volved  parts  be  excluded. 

Crepitation,  resembling  that  in  the  early  stage  of  lobar  pneumonia, 
and  audible  at  the  base  of  the  lung,  may  also  be  heard  in  cases  which 
later  develop  demonstrable  fluid.  Its  explanation  is  not  clear.  It  may 
be  ascribed  to  fine  pleural  friction,  to  air  entering  fluid  in  alveoli  under- 
lying an  inflamed  pleura,  and  to  expansion,  during  inspiration,  of  a 
slightly  retracted  and  atelectatic  lung,  giving  rise  to  crepitation 
coincident  with  the  separation  of  previously  apposed  alveolar  walls. 
A  similar  sound  may  also  be  heard  at  the  termination  of  the  disease, 
and  may  indicate  that  the  pleural  layers  are  again  approximated,  or 
that  air  is  again  admitted  to  the  base  of  the  lung. 

Breath  Sounds. — Changes  in  the  breath  sounds  in  uncomplicated 
pleural  effusion  are  due  to  several  factors,  more  than  one  of  which 
usually  operate  in  any  given  case.  They  depend  on  diminished  expan- 
sion of  the  lung,  from  spasm  or  paralysis  of  the  respiratory  muscles, 
to  changes  in  the  lung  itself  from  retraction  or  pressure,  and  to  the 
presence  in  the  pleural  cavity  of  fluid  which  modifies  or  may  even 
abolish  the  variations  conducted  from  the  lung  to  the  chest  wall. 

Early  in  the  disease  irritation  of  the  pleura  and  pain  diminish  the 
respiratory  murmur  from  spasm  of  the  respiratory  muscles  and  fixa- 
tion of  the  side.  Even  slight  exudation  without  pain  may  do  likewise 
from  the  mechanical  obstruction  of  fluid.  In  the  presence  of  fluid, 
however,  the  retraction  and  increased  density  of  the  lung  may  give 
rise  not  only  to  a  diminution  in  the  intensity  of  the  respiration,  but 
to  a  change  in  its  character.    With  small  effusions,  the  inspiration  is 


ACUTE  SEROFIBRINOUS  PLEURITIS  485 

merely  diminished,  while  expiration  is  abnormally  long,  somewhat 
higher  pitched,  and  slightly  bronchial  in  character.  As  the  fluid 
increases  in  amount,  the  breathing  over  the  base  of  the  lung  may 
have  a  distinctly  tubular  quality.  This  is  often  most  marked  in  the 
interscapular  region  above  the  level  of  the  fluid.  With  large  effusions 
the  breathing  is  vesicular  in  the  upper  part  of  the  chest.  It  may  be 
bronchial  above  and  absent  below  .the  level  of  the  fluid.  When  the 
lung  is  completely  retracted  and  compressed,  there  may  be  almost 
no  respiratory  murmur  over  the  affected  side.  At  times  the  breathing 
may  have  an  amphoric  character  in  the  upper  part  of  the  chest.  Kales, 
as  well  as  bronchial  breathing,  may  have  a  metallic  quality  and  thus 
suggest  cavity.  In  children  the  breathing  is  more  likely  to  be  bron- 
chial than  in  adults.  With  the  subsidence  of  the  effusion  the  vesicular 
breathing  returns,  but  may  for  long  or  even  permanently  remain 
somewhat  diminished.  As  the  atelectatic  lung  expands,  rales  can 
usually  be  heard.  An  accompanying  catarrh  or  edema  of  the  lungs 
may  give  rise  to  rales  on  the  side  of  the  effusion  which  may  have  a 
consonating  quality  from  pulmonary  compression.  The  breathing 
over  the  unaffected  lung  is  often  increased  with  prolongation  of  expira- 
tion. 

Voice  Sounds. — The  voice  sounds  are  often  increased  above,  dimin- 
ished or  absent  below  the  level  of  the  fluid.  The  voice  may  have  a 
peculiar  nasal  or  bleating  quality,  the  so-called  segophony.  It  is  most 
often  heard  in  the  posterior  and  lower  thoracic  regions.  The  whisper 
is  variable,  but  in  general  is  increased  over  the  region  where  bron- 
chophony is  heard,  and  may  have  a  bronchial  character.  It  is  usually 
diminished  or  absent  over  the  fluid.  It  is  said  by  Bacelli  to  be  trans- 
mitted through  a  serous  and  not  through  a  purulent  exudate,  but  the 
,  sign  is  not  reliable. 

Examination  of  the  Heart. — Dislocation  of  the  heart  is  one  of  the  most 
important  signs  of  pleural  effusion.  The  position  of  the  visible  cardiac 
impulse  should  be  noted.  It  may  be  seen  at  either  side  of  the  sternum. 
If  the  apex  is  behind  the  sternum,  there  may  be  no  visible  pulsation. 
At  times  an  impulse  is  seen  below  the  ensiform  in  the  upper  epigastric 
region.  Palpation  for  the  systolic  impulse  in  the  spaces  on  either  side 
of  the  sternum  may  furnish  more  definite  information.  In  some  cases 
pulsation  can  be  neither  seen  nor  felt,  and  reliance  must  be  placed 
on  auscultation.  Greene1  finds  that  rhythmic  lateral  displacement  of 
the  heart  is  a  sign  of  unilateral  pleural  fluid.  It  may  be  demonstrated 
by  inspection,  auscultatory  percussion,  or  the  fluoroscope.  A  systolic 
murmur  is  not  infrequently  heard  over  the  displaced  heart,  and  is  prob- 
ably due  to  pressure  on  the  great  vessels,  especially  the  pulmonary 
artery. 

Special  Physical  Signs. — 1.  Displacement  of  the  Heart. — (a)  Away 
from  the  Affected  Side. — An  accumulation  of  air,  fluid,  or  other  foreign 

1  Amer.  Jour.  Med.  Sci.,  1906. 


186  DISEASES  OF  THE  PLEURA 

material  in  one  pleural  sac  allows  the  lung  on  that  side  to  contract, 
and  thus  exhausts  a  part  of  its  elastic  force.  The  intrapleural  tension 
on  the  affected  side  is  correspondingly  increased,  while  that  on  the 
unaffected  side  is  still  maintained  at,  or  nearly  at,  its  former  level. 
The  mediastinum  is  thus  subjected  on  either  side  to  unequal  pressure, 
and  seeks  a  position  of  equilibrium  between  the  two.  Because  of  the 
firmness  with  which  the  mediastinum  as  a  whole  is  held  in  place  by 
ligamentous  bands  and  bloodvessels  branching  in  various  directions, 
its  displacement  is  less  marked  than  that  part  of  it  occupied  by  the 
heart,  which  is  attached  above  to  the  relatively  immobile  aorta,  but 
is  elsewhere  capable  of  considerable  lateral  motion  within  the  elastic 
parietal  pericardium.  It  seems  more  in  accordance  with  the  mechani- 
cal factors  to  regard  cardiac  displacement  as  due  to  a  thrust  or  "push" 
of  the  relatively  higher  intrapleural  pressure  in  the  diseased  sac  than  a 
"pull"  from  the  relatively  lower  pressure  in  the  normal  side. 

Provided  the  heart  is  free  to  move  laterally,  its  displacement  may 
be  one  of  the  first  signs  of  an  accumulation  in  the  pleural  sac.  The 
intrapleural  pressure  on  the  diseased  side  need  not  be  actually  posi- 
tive. Apposition  of  fluid  or  other  material  to  the  heart  is  not  a  neces- 
sary factor.  Because  of  the  normal  position  of  the  heart  on  the  left, 
it  is  always  displaced  a  greater  distance  to  the  right  with  left-sided 
pleural  disease  than  to  the  left  with  disease  of  the  right  pleura.  To 
judge  from  Carriere's  observations  and  experiments,  the  amount  of 
fluid  in  the  left  chest  may  reach  700  c.c.  without  displacement  of  the 
heart.  The  writer  has  seen  slight  cardiac  displacement  develop  under 
observation  in  a  girl  of  fourteen,  from  whose  left  pleura  250  c.c.  of 
pus  were  evacuated  by  operation.  Cardiac  dislocation  may  be  noted 
before  dilatation  of  the  side  is  evident.  As  much  as  1000  c.c.  of  fluid 
may  be  present  in  the  right  pleura  without  evident  displacement  of 
the  heart  to  the  left.  In  such  diseases  as  pneumonia,  in  which  pleural 
fluid  may  occur  as  a  complication,  or  in  cases  in  which  its  presence 
is  suspected,  a  careful  record  of  the  position  of  the  heart  may  be  of 
unexpected  value  later  in  the  course,  when  a  slight  deviation  from  its 
originally  recorded  position  may  be  a  deciding  factor  in  a  diagnosis, 
otherwise  doubtful  because  of  pulmonary  changes  complicating  the 
physical  signs.  Since  cardiac  displacement  depends  not  only  on  a 
loss  of  retractile  force  in  the  lung  on  the  diseased  side,  but  also  on  the 
maintenance  of  elastic  tension  in  the  opposite  lung,  any  interference 
with  the  latter  from  disease  will  correspondingly  limit  the  cardiac 
excursion  toward  that  side.  Thus  pleural  adhesions,  pneumonic 
infiltration,  emphysema,  or  other  structural  changes  may  so  diminish 
the  elastic  power  of  the  uncontracted  lung  as  to  limit  or  even  prevent 
cardiac  displacement. 

(6)  Toward  the  Affected  Side. — Occasionally  in  the  course  of  long 
continued  pleural  disease,  absorption  may  lead  to  an  increase  of  nega- 
tive pressure  on  the  diseased  side.  The  heart  may  then  be  pushed 
toward  this  side  by  the  relatively  greater  but  still  negative  pressure  in 


ACUTE  SEROFIBRINOUS  PLEURITIS  487 

the  unaffected  pleura.  Thus  far  mention  has  been  made  only  of  cardiac 
displacements  from  differences  of  intrapleural  pressure.  The  heart 
may,  however,  actually  be  pulled  to  one  side  by  the  contraction  of 
adhesions  between  it  and  neighboring  structures. 

(c)  Position  of  the  Displaced  Heart. — The  studies  of  Powell,  Ferber, 
Bard,  Pitres,  and  others  show  that  in  the  displacement  to  the  right 
with  left-sided  effusions  the  heart  practically  always  maintains  its 
position  with  the  apex  to  the  left  of  the  base,  pulsation  to  the  right 
of  the  sternum  arising  at  the  base  of  the  heart.  In  Lafforgue's1  case, 
however,  with  a  large  effusion  of  blood  in  the  left  pleural  sac,  the  heart 
was  found  at  autopsy  pointing  to  the  right. 

2.  Diaphragm  Phenomenon. — Gerhardt2  referred  to  this,  but  thought 
it  of  rare  occurrence  and  limited,  for  the  most  part,  to  emaciated 
individuals.  Litten3  observed  its  presence  in  all  normal  individuals, 
more  accurately  described  its  clinical  appearance,  and  emphasized  its 
importance  in  pathologic  conditions.  He  found  it  represented  in 
Michael  Angelo's  figure  of  the  dying  Adonis  in  the  court  of  the  Bar- 
gello  at  Florence. 

With  the  patient  and  the  observer  correctly  placed,  one  may  see 
in  practically  all  normal  individuals  a  transverse  shadow  descending 
with  inspiration  and  ascending  with  expiration  over  a  narrow  zone  in 
the  lower  anterior  and  lateral  regions  of  the  chest.  It  begins  above  in 
the  region  of  the  seventh  rib,  intersecting  the  ribs  at  an  acute  angle 
as  it  descends  on  deepest  inspiration  a  distance  of  two  to  three  spaces, 
or  about  6  to  7  cm.,  to  ascend  to  its  original  position  with  expiration. 
On  superficial  respiration,  its  amplitude  is  about  one  to  one  and  a  half 
spaces.  It  is  best  seen  between  the  axillary  and  mammary  lines,  but 
may.be  followed  through  the  axilla  and  the  back,  with  the  patient 
lying  on  the  abdomen.  It  is  highest  in  front,  descends  somewhat 
toward  the  axilla,  then  runs  in  a  nearly  horizontal  line  toward  the 
spine,  and  is  lost  between  the  angle  of  the  scapula  and  the  spinal 
column.  During  inspiration,  the  differences  of  pressure  in  the  thorax 
and  abdomen  are  expressed  on  the  thoracic  wall  as  a  horizontal  furrow. 
A  short  interval  elapses  between  the  beginning  of  inspiration  and  the 
appearance  of  the  phenomenon. 

The  sign  is  of  value  in  unilateral  pulmonary  or  pleural  disease.  It 
is  absent  in  pneumonia  of  the  lower  lobes,  is  diminished  in  amplitude 
or  absent  and  abnormally  low  in  the  presence  of  pleural  fluid  or  air. 
The  excursion  is  diminished,  distorted,  or  irregular  in  the  presence 
of  pulmonary  infiltration  (as  in  tuberculosis),  thoracic  retraction, 
following  pleural  or  pulmonary  disease,  pulmonary  or  pleural  tumors, 
and  with  pleural  adhesions.  With  enlargement  of  the  liver  or  spleen, 
with  abdominal  fluid  or  tympanites,  it  may  be  diminished  in  ampli- 
tude and  abnormally  high.  The  sign  may  be  of  assistance  in  the 
diagnosis  of  subphrenic  abscess,  simulating  suppuration  in  the  lower 

1  Gaz.  des  hop.,  1902.  2  Der  Stand  der  Diaphragmas,  Tubingen,  I860. 

3  Deut.  med.  Woch.,  1892,  and  Verhandl.  d.  Cong.  f.  inn.  Med.,  1S95. 


188  DISEASES  OF   THE  PLEURA 

thoracic  region.  The  presence  of  the  shadow  above  the  involved  area, 
although  of  diminished  amplitude,  may  indicate  the  subdiaphragmatic 

site  of  the  lesion.  It  is  also  of  value  in  distinguishing  pneumothorax 
from  diaphragmatic  hernia,  being  absent  in  the  former,  but  present 
in  the  latter. 

.'!.  Paravertebral  Triangle  of  Dulness.  The  presence  of  a  normal 
triangle  of  dulness  at  either  side  of  the  spinal  column  in  the  anterior 
thoracic  region  makes  the  pathologic  triangle  more  difficult  of  inter- 
pretation and  somewhat  limits  its  value  as  a  diagnostic  sign.  On 
percussion  of  the  spinal  column  from  above  downward,  the  note 
becomes  progressively  duller  as  its  lower  thoracic  limit  is  approached. 
The  degree  of  normal  dulness  in  this  region  can  be  appreciated  only 
by  experience. 

Koranyi's1  and  Grocco's  observations  on  this  sign  have  since  been 
confirmed  by  many  observers.  Specially  noteworthy  are  the  obser- 
vations of  Baduel  and  Siciliano2  on  its  explanation  and  the  series  of 
clinical  cases  studied  by  Thayer  and  Fabyan.3 

Having  determined  the  limits  of  a  suspected  effusion  by  percussion 
and  similarly  outlined  the  lowest  limit  of  pulmonary  resonance  on  the 
unaffected  side,  the  spinous  processes  of  the  vertebrae  are  percussed 
from  above  downward  and  the  point  noted  where  relative  dulness 
begins.  This  usually  corresponds  to  the  level  of  relative  dulness  on 
the  affected  side,  and  somewhat  higher  than  the  level  of  flatness. 
Percussion  of  the  unaffected  lung  in  horizontal  lines  toward  the  spinal 
column  discloses  a  paravertebral  area  of  relative  dulness  of  a  triangular 
shape.  The  vertical  side  of  the  triangle  coincides  with  a  line  drawn 
through  the  spinous  processes  of  the  vertebrae,  the  base  with  the  limit 
of  .pulmonary  resonance  on  the  sound  side.  Its  outer  side  is  formed 
by  a  line  extending  obliquely  downward  and  outward.  The  height 
of  the  vertical  and  the  width  of  the  base  line  vary  with  the  size  of  the 
effusion.  The  base  may  thus  vary  from  2  to  7  cm.  in  length.  The 
triangle  is  somewhat  larger  in  right-sided  effusions.  It  may  differ  from 
the  normal  triangle  only  in  the  degree  of  dulness.  In  Thayer  and 
Fa  by  an 's  series  a  small  but  distinct  triangle  was  detected  with  a  lefti 
sided  effusion,  which  on  tapping  disclosed  only  250  c.c.  of  serofibrinous 
fluid.  On  changing  the  position  of  the  patient  from  the  upright  to 
the  horizontal,  the  dull  triangle  nearly  or  quite  disappears  unless  the 
fluid  is  encapsulated.  The  respiratory  murmur,  the  voice  sounds, 
and  fremitus  are  diminished  over  this  area,  but  the  changes  are  less 
marked  than  on  the  affected  side.  The  character  of  the  fluid  appears 
not  to  influence  the  triangle. 

1  The  triangle  was  first  noted  by  Koranyi  in  1897  (in  the  fourth  volume,  p.  717,  of 
Belgogyaszat  Kezikonyze,  and  again  in  Eulenberg's  Realenzyklopiidie  der  gesamtem 
Heilkunde,  vol.  xiii).  It  was  independently  rediscovered  and  more  fully  described  by 
Grocco  (Riv.  crit.  di  clin.  med.,  Firenze,  1902). 

2  Riv.  crit.  di  med.,  Firenze,  1904,  v,  5,  21,  37. 

3  Amer.  Jour.  Med.  Sci.,  January,  1907. 


ACUTE  SEROFIBRINOUS  PLEURITIS 


489 


The  dull  triangle  is  practically  constant  in  the  presence  of  free 
pleural  fluid  or  of  encapsulated  fluid  in  contact  with  the  spinal  column. 

In  explanation  of  the  phenomenon,  Baduel  and  Siciliano1  suggest 
that  fluid  intervening  between  the  spine  and  resonant  lung  inhibits  the 
capacity  of  the  former  for  sonorous  vibrations,  thus  acting  as  a  mute. 
The  diminished  resonance  extends  into  the  paravertebral  region  and 
increases  in  width  from  above  downward,  since  the  fluid  at  its  base 
comes  into  wider  contact  with  the  spinal  column  and  extends  farther 
toward  the  opposite  side.  Displacement  of  the  mediastinal  contents 
and  compression  of  the  sound  lung  may  play  a  part  in  its  production. 

Fig.  79 


Aortic  insufficiency;    hydro  thorax  on  the  right  side;    paravertebral  triangle  of  dulness 
on  the  left.     (Thayer  and  Fabyan.) 


Paravertebral  Dulness  on  the  Affected  Side. — Free  pleural  effusions 
distend  the  pleural  sac  and  interrupt  spinal  vibrations  with  the  pro- 
duction of  dulness  on  one  or  both  sides  of  the  spine  according  to  the 
size  of  the  effusion.  If  the  effusion  is  small,  the  dulness  may  be  limited 
to  the  paravertebral  region  on  the  affected  side  without  evidence  of 
Grocco's  triangle  on  the  other.  With  pneumonia  affecting  the  lower 
lobes  and  uncomplicated  by  an  effusion,  on  the  other  hand,  a  zone 


Riv.  crit.  di  med.,  Firenze,  1904.  v,  5,  21,  37. 


490  DISEASES  OF   THE   PLEURA 

of  relative  resonance  about  two  fingers'  breadth  in  width  can  usually 
be  demonstrated  in  the  paravertebral  region  on  the  affected  side.' 
This  strip  of  relative  resonance  may  be  obvious  only  in  the  presence 
of  extensive  lobar  pneumonia  and  absent  or  doubtful  with  small  areas 
of  consolidation  from  other  causes.  It  is  probably  due  to  uninterrupted 
spinal  vibrations  reinforced  by  compensatory  emphysema  of  the 
unaffected  lung.  A  zone  of  dulness  in  the  paravertebral  region  on  the 
affected  side  with  pleural  effusion  and  relative  resonance  in  this  region, 
with  lobar  pneumonia  may  be  of  some  value  in  differentiating  the  two 
conditions. 

Blood. — The  number  of  red  cells  and  the  amount  of  haemoglobin 
present  no  striking  features  beyond  usually  not  more  than  slight 
grades  of  secondary  anaemia. 

White  Cells. — In  general,  it  may  be  said  that  the  leukocytes  in 
primary  serofibrinous  pleuritis  are  only  rarely  above  normal  in  the 
absence  of  complications.  Infectious  pleuritis,  on  the  other  hand, 
is  usually  accompanied  by  leukocytosis.  The  white  count,  therefore, 
may  be  of  value  in  distinguishing  the  two  forms  of  the  disease. 

Tuberculoid  Effusion. — Of  33  cases  of  primary  serofibrinous  pleuritis 
in  which  tubercle  bacilli  were  found  in  the  fluid  by  inoscopy  or  animal 
inoculation  the  white  count  was  above  12,000  in  only  3  (9  per  cent.), 
of  whom  2  showed  a  leukocyte  count  of  14,000  to  15,000,  and  the 
remaining  case  20,400.  A  complicating  pulmonary  tuberculosis  may 
raise  the  white  count,  for  of  32  cases  in  this  group  7  (21.8  per  cent.) 
were  12,000  or  over.  In  301  primary  cases,  of  probable  tuberculous 
nature,  the  white  count  was  12,000  or  over  in  57  (18.9  per  cent.). 
Of  these  57  cases  the  leukocytes  numbered  12,000  to  13,000  in  22; 
13,000  to  14,000  in  9;  14,000  to  15,000  in  8;  15,000  to  16,000  in  3; 
16,000  to  20,000  in  10,  and  20,000  to  24,000  in  5.  The  leukocytosis 
was  doubtless  transient  in  many. 

In  224  separate  counts,  in  20  cases  of  primary  pleurisy,  daily  until 
discharge  or  disappearance  of  the  fluid,  Morse2  found  that  only  13 
counts  went  above  10,000.  Of  these,  9  were  in  1  case  showing  pneu- 
mococcus  infection  at  autopsy.  The  other  4  were  in  2  cases,  and  the 
counts  were  but  little  above  10,000.  He  concludes  from  his  study 
that  there  is  no  evident  relation  between  the  duration  of  the  disease, 
the  temperature,  the  presence  of  blood  or  few  pus  cells  in  the  fluid, 
the  amount  of  fluid  or  its  variation  and  the  leukocyte  count. 

Infectious  (non-tuberculous)  Pleuritis. — The  metapneumonic  effu- 
sions, are,  as  might  be  expected,  accompanied  by  an  increase  of  the 
white  cells.  Of  28  cases  in  this  class  the  leukocytes  were  above  12,000 
in  all  but  6  (78.5  per  cent.).  They  numbered  12,000  to  16,000  in  4; 
16,000  to  20,000  in  6;  20,000  to  50,000  in  12.  Pneumonia  is  not  a 
necessary  factor  in  raising  the  white  count,  however,  and  infection  of 
the  pleura  alone  in  apparently  uncomplicated  cases  with  serofibrinous 

1  Lord,  Boston  Med.  and  Surg.  Jour.,  February  12,  1914,  p.  245. 

2  Amer.  Jour.  Med.  Sci.,  1900,  cxx,  658. 


ACUTE  SEROFIBRINOUS  PLEURITIS  491 

effusion  may  raise  the  white  count,  as  in  2  streptococcus  infections 
with  19,000  and  35,400  white  cells. 

Serofibrinous  effusions  complicating  arthritis  showed  an  increase 
of  white  cells  in  all  of  3  cases,  but  it  must  be  a  question  whether  the 
leukocytosis  can  be  ascribed  to  the  one  or  the  other  lesion. 

Differential  Count. — Aside  from  the  occasional  presence  of  eosino- 
philia  in  hemorrhagic  effusions,  there  appears  to  be  nothing  char- 
acteristic in  the  differential  count  in  serofibrinous  effusion.  Of  17 
cases,  the  relative  proportion  of  white  cells  showed  nothing  remark- 
alble  with  the  exception  of  a  relative  increase  in  the  poly  nuclear  cells 
in  cases  with  leukocytosis  and  an  eosinophilia  of  20  per  cent,  in  1  of 
5  cases  with  bloody  fluid. 

Spleen. — This  is  rarely,  if  ever,  enlarged  unless  some  complication 
exists.  It  may  be  palpable  from  dislocation  with  left-sided  accumu- 
lation. 

Axillary  Glands. — Due  allowance  must  be  made  for  the  presence  of 
small  palpable  glands  in  a  large  proportion  of  normal  individuals. 
Rarely  the  axillary  glands  on  the  affected  side  may  be  enlarged  by 
extension  of  the  pleural  disease,  whether  simple,  tuberculous  or  malig- 
nant. 

Inequality  of  the  Pupils. — This  may  in  rare  instances  occur  from 
involvement  of  the  sympathetic  nerve.  The  difference  in  size  is 
usually  slight. 

Blood-pressure. — This  is  usually  normal  with  pleural  effusions,  com- 
pensation for  intrathoracic  pressure  being  maintained  by  increased 
respiration.  When  this  compensation  fails,  however,  there  may  be  a 
fall  of  pressure.  Capps1  noted  an  increase  of  blood-pressure  during 
the  excitement  preceding  thoracentesis.  There  was  a  constant  fall 
during  the  withdrawal  of  the  fluid,  the  average  in  19  observations 
being  20  mm.  Hg.  Evacuation  of  large  amounts  of  fluid,  rapid  with- 
drawal, long  duration  of  the  effusion,  senile  changes  in  the  blood- 
vessels and  heart,  increased  the  fall  of  pressure. 

Radioscopy. — This  may  confirm  the  results  of  physical  examination, 
showing  the  limits  of  the  effusion,  the  position  of  the  displaced  heart 
and  the  diaphragm.  It  may  also  show  the  presence  of  unsuspected 
pulmonary  processes.  It  is  especially  valuable  in  locating  an  encap- 
sulated effusion.  The  fluoroscope  admits  of  examination  from  differ- 
ent points  of  view  in  rapid  succession,  but  the  radiograph  is,  in  general, 
to  be  preferred.  Permanent  records,  for  study  and  comparison,  are 
thus  secured.  The  plates  are  most  satisfactory  if  the  patient  can 
hold  his  breath  during  the  exposure.  Pleural  adhesions  may  be  sug- 
gested by  a  lack  of  diaphragmatic  excursion.  Thick  pleura  without 
fluid  may  be  indicated  by  a  lack  of  uniformity,  by  irregular  limitation 
of  the  shadow  and  an  absence  of  depression  of  the  diaphragm  and  dis- 
location of  the  heart.    The  shadow  is  less  dense  than  with  fluid.    In 

1  Jour.  Amer.  Med.  Assoc,  January  5,  1907. 


492 


DISEASES  OF   THE   PLEIL'A 


the  presence  of  pleural  fluid,  the  shadow  is  more  uniform,  more  sharply 
outlined,  and  when  the  fluid  is  free  occupies  the  lower  part  of  the  pleural 
space.  Its  upper  border  is  curved,  unless  pneumothorax  is  present, 
when  it  assumes  a  hydrostatic  level.  A  comparison  of  plates  taken 
with  the  patient  upright  and  lying  down  confirms  the  clinical  observa- 
tion of  the  mobility  of  fresh  serofibrinous  effusions.  The  shadow 
produced  by  serous  is  less  dense  than  by  purulent  or  hemorrhagic 
fluid. 

Fiu.  SO 


Pleurisy  with  left-sided  purulent  effusion.    The  entire  left  side  of  the  chest  is  opaque  on 
comparison  with  the  right.    Displacement  of  the  heart  to  the  right.    (No.  188,395.) 


Complications. — Lesions  having  an  etiologic  relation  with  the  dis- 
ease have  already  been  considered.  It  is  difficult  oftentimes  during 
life  or  even  at  the  postmortem  table  to  separate  them  from  conditions 
dependent  on  the  pleuritis.  These  secondary  processes,  only  need 
be  considered  here.  Tuberculosis  may  rarely  extend  from  pleura  to 
uninvaded  lung.  The  progress  is  usually,  however,  from  lung  to 
pleura.  Acute  miliary  tuberculosis  may  rarely  complicate  or  follow7 
serofibrinous  effusion.  Infection  may  extend  to  the  opposite  pleura, 
the  pericardium,  peritoneum,  or  other  parts  of  the  body.  Perihepatitis 
or  perisplenitis  may  thus  arise.  Thrombosis  of  the  pulmonary  vessels, 
the  vense  cavse,  heart,  iliac,  femoral,  saphenous,  or  other  veins  may 


ACUTE  SEROFIBRINOUS  PLEURITIS  493 

be  associated  with  increased  intrathoracic  pressure  and  infection. 
Embolism  may  be  rapidly  fatal.  Edema  of  the  lungs  is  a  constant 
danger  in  large  accumulations  and  with  untapped  effusions  is  prob- 
ably due  to  cardiac  insufficiency.  Perforation  of  the  lung  or  thoracic 
wall  complicates  purulent  effusions  with  unfortunate  frequency,  but 
is  rare  with  the  serofibrinous  form.  Serous  expectoration  without 
relation  to  thoracentesis  has  been  noted  by  Scriba,1  Sahli,2  and 
Appel.3  Nephritis  probably  bears  only  a  chance  relation  to  pleuritis. 
It  arose  under  observation  in  only  1  of  500  cases  in  the  writer's 
series. 

Causes  of  Sudden  Death. — Death  may  be  due  to  associated  and  inde- 
pendent lesions  to  which  the  pleuritis  is  secondary.  Such  causes  need 
not  be  considered  here.  Of  causes  dependent  on  the  serofibrinous 
effusion,  thrombosis  and  embolism  are  among  the  most  frequent. 
The  pulmonary  vessels,  the  auricles,  the  venae  cava?,  iliac  and  femoral 
veins  often  contain  thrombi,  which  may  give  rise  to  emboli,  with 
rapidly  fatal  pulmonary  embolism,  as  in  5  of  14  autopsies  in  this 
series.  Cerebral  embolism  is  less  common.  Edema  of  the  lungs  may 
be  the  only  associated  lesion  found,  as  in  one  case  with  a  double 
effusion.  Postmortem  examination  does  not  always  disclose  the 
immediate  cause  of  death,  which  has  then  been  thought  to  be  due 
to  compression  of  the  aorta  (Trousseau),  or  to  a  kink  or  twist  in  the 
inferior  vena  cava  (Bartels),  but  Osier  in  a  number  of  observations 
was  unable  to  substantiate  the  latter.  Cerebral  anemia,  from  a 
mechanical  hindrance  to  the  circulation,  is  a  possible  cause.  Pressure 
on  the  venae  cavse,  and  the  heart  itself,  especially  the  auricles,  may 
embarrass  the  cardiac  mechanism,  resulting  not  only  in  cyanosis, 
rapid,  feeble  pulse,  and  dyspnea,  but  even  syncope  and  death.  Various 
factors  may  operate  in  individual  cases.  Large  double  or  left-sided 
effusions  are  more  dangerous.  Death  may  follow  sudden  changes  of 
position,  an  attack  of  pain,  deep  respiration,  or  a  paroxysm  of  cough. 
Many  more  lives  are  sacrificed  by  hesitation  and  delay  in  thoracentesis 
than  by  the  operation. 

Duration. — Of  369  cases  of  primary  serofibrinous  pleuritis,  the 
time  from  the  beginning  of  symptoms  to  discharge  from  the  hospital 
was  less  than  three  weeks  in  53,  three  to  six  weeks  in  167,  six  to. nine 
weeks  in  60,  nine  to  twelve  weeks  in  43,  three  to  six  months  in  31, 
six  months  to  one  year  in  12,  two  years  or  over  in  3.  Thus,  about 
60  per  cent,  ran  their  course  within  six  weeks,  about  87  per  cent, 
within  three  months.  The  duration  is  longer  with  large  effusions,  in 
old  and  debilitated  patients,  in  the  presence  of  complications,  in 
untapped  cases  or  those  in  which  evacuation  is  delayed.  It  is  shortest 
in  primary  effusions,  in  young  and  otherwise  apparently  healthy 
individuals,  treated  by  early  tapping. 

1  Deut.  Arch.  f.  klin.  Med.,  1886,  xxxvi,  329. 

2  Mitth.  a.  klin.  u.  med.  Inst.  d.  Schweitz.,  1894. 

3  Munch.  Annalen,  1897,  Fall  15. 


I'.M  DISEASES  OF   TIIK  PLEURA 

Relapse.  -Although  it  is  not  uncommon  after  withdrawal  of  fluid 
tor  it  to  reaccumulate  under  observation  and  necessitate  one  or  more 
tappings,  it  is  rare  for  a  serofibrinous  effusion  to  reappear  on  the  same 
side  after  it  has  been  fully  absorbed  or  removed.  In  one  of  my  series, 
nine  months  elapsed  between  the  removal  of  fluid  and  the  appear- 
ance of  the  patient  with  an  accumulation  on  the  same  side,  but  it 
is  not  certain  that  the  fluid  was  fully  removed  at  the  first  operation. 
The  obliteration  of  the  pleural  sac  following  serofibrinous  effusion  is 
probably  responsible  for  the  rarity  of  true  relapse. 

Sequelae. — It  is  rare  for  serofibrinous  effusions  to  change  from 
serous  to  purulent  fluid.  Of  1185  cases,  empyema  developed  in  only 
16  (1.3  per  cent.).  When  empyema  follows  serofibrinous  effusion,  the 
fluid  has  usually  been  turbid,  with  an  excess  of  polynuclear  cells 
from  the  beginning.  Spontaneous  or  artificial  pneumothorax  may 
occur,  and,  if  the  communication  is  through  the  lung,  infection  may 
follow.  Imperfect  technic  in  tapping  may  cause  empyema.  Slight 
dulness,  diminished  expansion,  breathing,  and  fremitus  last  for  a 
variable  period  after  the  disappearance  of  serofibrinous  fluid.  The 
intercostal  spaces  may  be  slightly  narrowed  and  the  affected  side 
somewhat  smaller.  These  changes  may  be  permanent,  but  are  less 
common  and  less  marked  than  after  empyema.  The  heart  usually 
returns  to  its  normal  position.  Rarely  it  may  be  fixed  by  adhesions 
in  an  abnormal  position  toward  the  sound  side  or  slightly  displaced 
toward  the  affected  pleura.  Slight  lateral  deviation  of  the  spine  may 
accompany  these  changes. 

Diagnosis. — This  is  usually  easily  made  from  the  onset  with  pain, 
the  diminution  or  disappearance  of  which  is  accompanied  by  increas- 
ing dyspnea,  the  diminished  expansion  of  the  affected  side,  initial 
narrowing,  with  later  enlargement  of  the  side  and  widened  interspaces, 
the  character  and  distribution  of  the  dulness,  diminished  or  absent 
breathing  and  fremitus,  and  the  displacement  of  neighboring  organs. 

Diseases  with  Which  an  Effusion  may  be  Confused. — 1.  Intrathoracic. 
(a)  Thick  Pleura. — Following  the  partial  or  complete  absorption  or 
removal  of  pleural  fluid,  the  thickened  pleura  may  give  rise  to  some 
confusion.  There  may  be  slight  dulness,  diminished  breathing  and 
fremitus.  The  side  is  not  flat,  however,  the  breathing  only  slightly 
altered,  without  bronchial  character,  and  the  fremitus,  although  it 
may  be  diminished,  is  not  absent.  The  paravertebral  triangle  of  dul- 
ness opposite  the  affected  side  is  absent  and  the  heart  is  not  displaced. 

(6)  Pneumonia. — Typical  lobar  pneumonia  is  easily  differentiated 
by  its  more  severe  onset,  with  chill  and  rapid  rise  of  temperature, 
cough  with  rusty  sputum,  dulness  (not  flatness),  bronchial  breath- 
ing, increased  voice,  whisper  and  tactile  fremitus,  and  consonating 
rales.  The  signs  are  often  confined  to  parts  or  the  whole  of  one  or 
more  lobes.  Atypical  pneumonia  may  closely  simulate  effusion. 
( !ough  and  expectoration  may  be  absent.  Partial  or  complete  involve- 
ment of  the  lower  lobes  with  occlusion  of  the  bronchi  by  secretion 


ACUTE  SEROFIBRINOUS  PLEURITIS  495 

(massive  pneumonia)  may  give  rise  to  signs  of  effusion.  If  the  bronchi 
can  be  emptied  by  cough,  the  signs  of  pneumonia  may  then  become 
clear.  The  absence  of  cardiac  displacement  is  important.  A  narrow 
strip  of  relative  resonance  in  the  paravertebral  region  on  the  affected 
side  with  croupous  pneumonia  and  dulness  in  this  region  with  pleural 
effusion  is  of  some  value  in  differentiating  the  two  conditions.  Small 
amounts  of  pleural  fluid  often  complicate  pneumonia.  Small  effu- 
sions are  more  often  serofibrinous,  large  amounts  more  commonly 
purulent.  In  doubtful  cases  exploratory  puncture  should  not  be 
delayed.  Chronic  suppurative  changes  in  the  lungs,  with  multiple 
bronchiectatic  cavities,  interstitial  pneumonia  and  thick  pleura,  may 
closely  resemble  pleural  effusion.  The  vocal  fremitus  may  be  dimin- 
ished; in  rare  instances  it  may  be  absent,  if  the  dilated  bronchi  are 
filled  with  secretion.  Evacuation  may  be  followed  by  a  return  of 
fremitus.  The  dulness  is  often  greater  in  some  places  than  in  others, 
and  is  not  as  marked  as  with  fluid.  The  side  may  be  contracted,  the 
interspaces  somewhat  narrowed,  and  the  heart  in  normal  position 
or  slightly  displaced  toward  the  affected  side.  The  diaphragm  may 
be  elevated,  the  diaphragm  phenomenon  diminished  in  amplitude 
or  absent.  Exploratory  puncture  is  attended  with  some  danger  of 
perforating  the  elevated  diaphragm  and  infection  of  the  peritoneum, 
of  bleeding  from  injured  bloodvessels  or  granulation  tissue,  or  the 
infection  of  an  intact  pleura  in  the  withdrawal  of  the  trocar.  If  pus 
is  found,  it  may  come  from  pulmonary  cavities. 

(c)  Tumors  of  the  Lung  and  Pleura. — Tumors  which  reach  the 
periphery  of  the  lung  may  give  rise  to  some  confusion.  There  may  be 
flatness,  diminished  or  absent  breathing,  and  fremitus.  The  site 
and  contour  of  the  process  may  differ  from  pleural  fluid.  Bloody 
sputum,  dyspnea,  stridor,  paralysis  of  the  vocal  cords,  dysphagia, 
dilatation  of  the  cervical  or  thoracic  veins  and  superficial  metastases 
may  be  suggestive.  If  the  pleura  is  invaded  by  the  new  growth,  an 
effusion  is  common  and  this  may  mask  the  pulmonary  process.  Explo- 
ratory puncture  may  evacuate  bloody  fluid.  Echinococcus  of  the 
lung  or  pleura  may  simulate  serofibrinous  pleuritis. 

(d)  Pericarditis  with  Effusion. — This  may  offer  some  difficulty  of 
differentiation  from  an  encapsulated  pleural  effusion  in  the  left  antero- 
lateral region.  The  same  symptoms  —  pain,  cough  and  dyspnea — 
may  be  present  in  both  conditions,  and  on  inspection  the  left  side 
of  the  chest  may  show  restricted  expansion.  Dulness  or  flatness, 
diminished  or  absent  respiration,  voice,  whisper  and  tactile  fremitus 
may  be  present  over  the  left  anterolateral  part  of  the  chest.  The 
following  features,  however,  may  serve  to  suggest  pericardial  rather 
than  pleural  effusion:  a  history  of  rheumatism  preceding  or  accom- 
panying the  onset  of  the  affection,  a  greater  degree  of  cyanosis  than 
might  be  expected  with  a  pleural  effusion  of  similar  size,  dilated 
cervical  veins,  paradoxical  pulse,  feeble  or  absent  cardiac  shock,  an 
obtuse  cardiohepatic  angle  on  percussion,  a  pyriform  or  oval  contour 


496 


DISK  ASKS   OF    THE    PLEURA 


to  the  dull  area  with  dulness  at  the  left  of  the  sternum  as  high  as  the 
second  rib,  declining  sharply  toward  the  left  axillary  region,  dulness 
in  the  left  infrascapular  region,  pericardial  friction  and  feeble  heart 
sounds.  Examination  by  means  of  the  arrays  may  be  of  great  value 
in  the  differentiation. 

2.  Abdominal  Affections. — Subdiaphragmatic  abscesses  and  tumors, 
especially  echinococcus  cysts,  may  simulate  an  accumulation  of  pleural 
fluid.  Abdominal  pain,  tenderness,  and  muscular  spasm  may  be  due 
to  diaphragmatic  pleurisy. 

Fiu.  81 


Subdiaphragmatic  abscess  of  the  right  side.  The  dome-like  elevation  of  the  dia- 
phragm is  indicated  as  an  opaque  shadow  with  convex  upper  margin  at  the  base  of  the 
right  lung.  The  costophrenic  sinus  is  obscured  by  a  slight  accumulation  of  pleural  fluid. 
(No.  191,899.) 


Subdiaphragmatic  abscess  may  present  special  difficulty  of  differ- 
entiation. Preceding  abdominal  symptoms  may  suggest  the  possi- 
bility of  abdominal  suppuration.  Among  the  numerous  causes, 
appendicitis,  pylephlebitis,  hepatic  abscess  in  connection  with  cholan- 
gitis with  or  without  gall-stones,  tropical  abscess  and  actinomycosis, 
perforated  gastric  or  duodenal  ulcer,  suppuration  in  or  about  the 
pancreas,  salpingitis  and  disease  of  the  kidney  or  spine  may  be  men- 
tioned. In  some  cases  preceding  abdominal  symptoms  are  lacking. 
Cough  and  expectoration  are  likely  to  be  absent.  The  right  side  is 
more  often  affected  than  the  left.     The  diaphragm  may  be  elevated 


ACUTE  KEROFIBIUNOUH  PLEURITJS 


497 


far  into  the  chest  or  intrude  only  slightly  into  the  lower  thoracic  aper- 
ture. In  cases  uncomplicated  by  pleural  effusion,  the  dome-like 
elevation  of  the  diaphragm  may  be  outlined  on  percussion  as  a  dull 
area  at  the  base  of  the  lung  with  convex  upper  margin.  An  impor- 
tant feature  in  the  percussion  outline  is  the  maintenance  of  resonance 
on  the  affected  side  in  the  paravertebral  region  which  is  dull  in  the 
presence  of  free  pleural  effusion.    Over  the  dull  area  the  breathing  is 

Fig.  82 


Subdiaphragmatic  abscess  complicated  by  secondary  pleurisy  with  purulent  effusion. 
The  entire  right  side  is  more  opaque  than  the  left.  The  more  transparent  apical  portion 
shades  gradually  into  a  more  dense  middle  zone  representing  pleural  fluid.  In  the 
lower  third  of  the  right  side  is  a  dense  opaque  shadow  with  convex  upper  margin,  repre- 
senting the  subdiaphragmatic  abscess.  The  upper  margin  of  the  elevated  diaphragm 
is  partially  obscured  by  the  pleural  effusion.  Displacement  of  the  heart  to  the  left. 
(No.  187,058.) 


diminished  and  may  have  a  bronchial  quality  from  pulmonary  retrac- 
tion or  compression.  The  voice  sounds  are  diminished,  but  do  not 
have  the  segophonic  quality  so  often  heard  with  pleural  effusion. 
The  tactile  fremitus  is  diminished  but  not  absent.  A  friction  rub 
may  be  heard  if  fibrinous  pleurisy  is  present.  The  heart  is  less  dis- 
placed than  with  pleural  effusion  of  corresponding  size.  If  a  com- 
plicating pleural  effusion  is  present,  the  signs  are  those  of  this  condition. 
Exploratory  puncture  may  demonstrate  the  presence  of  pus.  Sero- 
32 


498  DISEASES  OF  THE  PLEURA 

fibrinous  fluid  may  be  obtained  from  the  pleura  and  pus  from  below 
the  diaphragm.  Inspiratory  depression  of  the  point  of  the  needle  may 
indicate  that  the  diaphragm  has  been  perforated.  If  the  respiratory 
changes  of  tension  are  noted,  an  increase  of  pressure  may  be  demon- 
strated during  inspiration  and  a  diminution  of  pressure  during  expira- 
tion. X-ray  examination  furnishes  the  most  important  evidence. 
By  this  means  an  abrupt  dome-like  elevation  of  the  diaphragm  may 
be  seen  as  a  dense  shadow  with  convex  upper  border  at  the  base  of  the 
lung  (Fig.  81).  In  the  absence  of  a  complicating  pleural  effusion  a  clear 
space  is  observed  at  the  costophrenic  sinus  and  toward  the  mid-chest. 
Fluoroscopic  examination  usually  shows  a  greater  degree  of  inspira- 
tory depression  and  expiratory  elevation  of  the  diaphragm  than  is 
present  with  pleural  effusion.  If  a  complicating  pleural  effusion  is 
present  the  a*-ray  picture  is  obscured,  but  the  outline  of  the  elevated 
diaphragm  may  still  be  seen  through  the  shadow  caused  by  the  effu- 
sion (Fig.  82)  . 

Determination  of  the  Character  of  Pleural  Fluid. — This  is  impossible 
in  most  instances  without  exploratory  puncture,  but  certain  suggestive 
features  may  be  mentioned.  Hydrothorax  is  most  easily  distinguished 
from  the  presence  of  cardiac  or  renal  disease  or  both,  bilateral  fluid, 
which  shifts  more  readily  on  changing  the  position  of  the  patient,  and 
edema  elsewhere,  as  well  as  absence  of  pain,  fever,  leukocytosis,  and 
friction  rub.  In  unilateral  hydrothorax  without  general  dropsy  the 
distinction  may  be  impossible.  Hemorrhagic  fluid  may  be  suspected 
following  trauma,  when  the  effusion  is  secondary  to  malignat  disease, 
or  with  an  eosinophilia  in  the  circulating  blood.  Chylothorax  can 
hardly  be  distinguished,  but  may  be  suspected  with  the  known  pres- 
ence of  chylous  ascites.  Empyema,  in  typical  cases,  may  be  differ- 
entiated. It  is  more  likely  to  be  secondary  and  metapneumonic, 
while  serofibrinous  effusion  is  much  more  likely  to  be  primary.  If 
the  patient  is  a  child  and  under  five  years,  the  chances  are  much  in 
favor  of  pus.  The  symptoms  are  of  little  assistance  in  individual  cases, 
but  in  general  are  more  severe  in  empyema,  with  higher  and  more 
irregular  fever,  chills,  sweats,  and  more  rapid  loss  of  flesh,  strength 
and  color.  Edema  of  the  skin,  dilatation  of  the  superficial  veins, 
thoracic  pulsation,  perforation  of  the  lung  or  other  organs  may  sug- 
gest empyema.  A  leukocytosis  above  12,000,  unexplained  by  other 
features,  suggests  an  infectious  process  and  usually  means  pus. 

Exploratory  Puncture.  —  This  may  be  done  without  pain  as  fol- 
lows: The  site  of  the  puncture  is  frozen  with  ethyl  chloride  spray. 
The  syringe  is  filled  with  about  2  c.c.  of  sterile  water  containing 
gr.g-  (0.021  gm.)  novocain  and  gr.  21117  (0.00032  gm.)  adrenalin  and 
the  needle  introduced  through  the  frozen  area.  The  needle  is  thrust 
inward  by  degrees,  perpendicular  to  the  surface,  each  advance  being 
preceded  by  the  injection  of  a  small  amount  of  the  fluid  into  the  tissue 
in  front  of  the  point.  The  rib  is  passed  close  to  the  upper  margin  to 
avoid  the  intercostal  artery.     After  the  pleural  sac  is  reached,  the 


ACUTE  SEROFIBRINOUS  PLEUBITIS  499 

syringe  should  still  contain  some  fluid  which  may  then  be  used  to 
dislodge  from  the  lumen  of  the  needle  any  fibrin  or  other  material 
preventing  aspiration.  Thick  pus  may  fail  to  flow  through  a  small 
needle. 

In  addition  to  the  determination  of  fluid,  the  operator  may  appre- 
ciate any  unusual  thickness  or  density  of  the  pleural  or  pulmonary 
tissue  by  the  amount  of  resistance  encountered  by  the  instrument 
(palpatory  puncture).  In  rare  instances  a  diagnosis  between  pleural 
and  subdiaphragmatic  fluid  may  be  made.  By  the  removal  of  the 
syringe  and  the  attachment  of  a  rubber  tube  to  the  needle,  the  appa- 
ratus is  converted  into  a  siphon  and  the  amount  of  pleural  pressure 
may  be  determined,  as  suggested  by  Kronig.  The  normal  depression 
during  inspiration  and  elevation  during  expiration  of  the  column  of 
fluid  may  be  reversed  in  subdiaphragmatic  collections.  The  with- 
drawal of  small  amounts  of  fluid  by  exploratory  puncture  is  occasion- 
ally followed  by  rapid  spontaneous  absorption  of  what  remains. 

In  rare  instances,  if  the  needle  is  used  for  exploratory  puncture, 
the  microscopic  examination  of  a  piece  of  tissue  caught  in  the  lumen 
may  furnish  the  diagnosis.  In  one  of  my  series  a  tubercle  was  thus 
demonstrated.  Prentiss1  made  the  diagnosis  of  sarcoma  and  Steele 
and  Girvin2  of  carcinoma  of  the  pleura  by  this  means. 

Examination  of  Pleural  Fluids. — Under  normal  conditions  there  is 
merely  enough  pleural  fluid  to  lubricate  the  apposing  surfaces  of  the 
pleura?,  and  as  yet  no  chemical  analysis  of  this  has  been  made. 

1 .  Chemistry.  —  Pleural  fluid  may  be  serous;  it  may  contain 
varying,,  amounts  of  fibrin,  when  it  is  known  as  serofibrinous;  it  may 
also  vary  in  its  content  of  blood  and  pus  and  may  then  be  termed 
hemorrhagic,  fibrinopurulent,  or  purulent.  The  presence  of  chyle 
justifies  the  term  chylous;  of  fat  not  due  to  chyle,  chyliform.  Clear 
serous  fluids  are  usually  yellowish,  often  reddish  from  the  admixture 
of  blood,  and  at  times  somewhat  greenish  in  color.  Large  quantities 
of  blood  or  pus  are  usually  sufficiently  obvious  from  the  gross  appear- 
ance. 

Transudates  and  Exudates. — It  is  customary  to  make  a  clinical 
distinction  between  fluids  resulting  from  hydremia  and  stasis  or 
transudates  and  those  arising  in  the  course  of  inflammatory  processes 
or  exudates.  Such  fluids  may  be  due  to  one  or  more  different  factors, 
as  in  similar  accumulations  elsewhere.  It  will  suffice  here  merely  to 
refer  to  the  probable  influence  of  filtration  and  osmosis  and  an  increased 
permeability  or  possible  secretory  power  of  diseased  capillary  walls, 
concerning  the  ultimate  bearing  of  which,  however,  little  is  definitely 
known.  The  chemistry  is  of  principal  interest  in  furnishing  data 
which  may  confirm  a  clinical  diagnosis  of  hydremia,  stasis,  or  inflam- 
mation as  a  cause. 

In  general,  transudates  are  of  relatively  low  specific  gravity  and 

1  Trans.  Assoc.  Amer.  Phys.,  1893.  2  Proc.  Path.  Soc.  Phil.,  1901. 


500  DISEASES  OF   THE  PLEURA 

contain  a  small  amount  of  albumin,  i.  e.,  a  specific  gravity  of  1010  or 
under  for  hydremic'  fluids,  with  traces  to  1  per  cent,  of  albumin; 
and  1010  to  101.")  in  venous  transudates,  with  1  to  3  per  cent,  of  albu- 
min. The  albumin  is  principally  serum  albumin,  serum  globulin, 
and  a  trace  of  fibrinogen.  Only  a  very  slight  precipitate  follows  the 
addition  of  a  few  drops  of  acetic  acid  to  the  fluid.  It  coagulates  slowly 
or  not  at  all,  unless  mixed  with  blood.  The  specific  gravity  of  exu- 
dates, on  the  other  hand,  is  usually  1018  or  higher,  with  4  per  cent, 
or  more  of  albumin.  They  show  a  more  abundant  precipitate  on  the 
addition  of  acetic  acid,  contain  a  larger  amount  of  fibrinogen,  and 
usually  coagulate  rapidly  with  or  without  the  presence  of  blood. 
For  the  estimation  of  albumin  Esbach's  test  may  be  used,  but  is  only 
approximately  accurate,  and  for  more  exact  determination  more 
complicated  methods  must  be  employed,  such  as  the  weight  of  the 
precipitated  proteid  or  the  total  nitrogen  (Kjeldahl). 

2.  Cytology.  —  Cytodiagnosis. — By  this  is  understood  the  deter- 
mination of  the  cause  of  the  effusion  from  the  character  and  numeri- 
cal relation  of  its  cellular  elements. 

Technic. — The  fluid  should  be  examined  as  soon  as  possible  after 
withdrawal.  To  prevent  spontaneous  coagulation  and  the  entangle- 
ment of  cells  in  the  meshes  of  fibrin,  it  may  be  placed  at  once  in  a 
sterile  flask  containing  about  one-third  to  one-half  its  volume  of  1 
per  cent,  sodium  citrate  in  0.85  per  cent,  salt  solution.  If  coagulation 
has  already  occurred,  Widal  recommends  agitation  with  glass  beads 
to  dislodge  entangled  cells,  but  such  a  procedure  may  give  less  accurate 
results  than  the  examination  of  fluid  in  which  clotting  has  not  taken 
place.  The  sediment  is  obtained  by  centrifugalization,  the  super- 
natant fluid  carefully  decanted,  and  thin  smears  made  with  the  plati- 
num loop.  These  are  allowed  to  dry  in  the  air  or  over  the  Bunsen 
flame.  Care  must  be  taken  not  to  burn  the  preparation.  Wright's1 
blood  stain  is  allowed  to  remain  on  the  cover-glass  from  one-half  to 
one  minute,  then  diluted  with  8  to  10  drops  of  water,  and  allowed  to 
stand  one  to  two  minutes.  The  preparation  is  washed  in  a  gentle 
stream  of  tap  water,  dried  over  the  Bunsen  flame,  and  mounted  in 
balsam. 

Red  cells  are  of  relatively  little  importance  in  the  microscopic 
examination.  A  differential  count  should  be  made  of  the  white  cells, 
which  may  be  classed  as  follows: 

A.  Poly  nuclear:  (a)  Neutrophils;  (b)  Eosinophils;  (c)  Mast- 
cells. 

B.  Mononuclear:  (a)  Lymphocytes;  (6)  Endothelial  cells;  (c) 
Cells  intermediate  and  indistinguishable  from  (a)  and  (b). 

Polynuclear  neutrophils  correspond  to  similar  cells  found  in  the 
circulating  blood.  Degenerative  processes  may  lead  to  the  formation 
of  isolated  nuclear  fragments,  with  or  without  a  granular  protoplasm, 

1  Jour.  Med.  Research,  January,  1902. 


ACUTE  SEROFIBRINOUS  PLEURITIS 


501 


contraction  of  the  nucleus  alone  or  both  nucleus  and  protoplasm,  and 
vacuolization.  Such  changes,  however,  seldom  modify  the  character 
of  the  cells  to  such  an  extent  as  to  prevent  their  recognition.    Eosino- 


Fig.  83 


Lymphocytosis.     Case  of  primary  tuberculous  pleurisy.      X  750.     (Musgrave.) 

Fig.  84 


Large  phagocytic  endothelial  cells  and  polynuclear  leukocytes.     Case  of  acute 
infectious  pleurisy.      X  750.     (Musgrave.) 


502 


DISEASES  OF  THE  PLEURA 


philes  are  often  found  in  small  numbers,  mast-cells  less  often.  Both 
are  in  most  instances  readily  classified.  Of  the  mononuclear  cells, 
typical  examples  of  lymphocytes  and  endothelial  cells  are  easily 
differentiated.  The  lymphocytes  correspond  to  similar  cells  in  the 
blood.  At  times,  no  rim  of  protoplasm  can  be  detected  about  them. 
Endothelial  cells  are  large,  flat,  irregular,  round,  or  oval  in  contour, 
with  a  round  or  oval  blue  nucleus,  which  is  poor  in  chromatin  and 
often  vacuolated.  They  may  be  isolated  or  in  plaques,  the  so-called 
"Placards  endotheliaux."  Such  an  arrangement  as  the  latter  plainly 
indicates  their  origin  from  the  pleural  wall.  They  are  phagocytic, 
and  have  in  consequence  been  called  macrophages.  Considerable 
variation  is  common  in  nucleus  and  protoplasm.  Either  or  both  may 
be  markedly  vacuolated  and  one  or  the  other  may  be  absent. 

Fig.  85 


Endothelial  plaques  and  cells.    Case  of  hydro  thorax  due  to  cardiac  disease.     X  750. 

(Musgrave.) 


Unfortunately,  between  typical  examples  of  lymphocytes  and 
endothelial  cells  there  are  atypical  forms  of  mononuclear  leukocytes 
which  cannot  be  fairly  classed  with  either  of  the  two  groups.  Such 
atypical  cells,  however,  usually  comprise  but  a  small  proportion  of 
the  white  cells,  and  may  thus  introduce  a  negligible  error  in  the  dif- 
ferential counts.  In  some  cases,  the  classification  of  the  cellular 
elements  is  impossible  because  of  degenerative  changes. 

Cytologic  Formula. — The  varying  character  of  cells  in  pleural 
fluids  was  first  noted  by  Ehrlich.  Further  observations  were  made, 
among  others,  by  Quincke  and  Wolff.    In  1900,  Widal1  elaborated  the 

1  Widal  and  Ravaut,  Compt.-rend.  de  la  Soc.  de  Biol.,  1900,  p.  648. 


ACUTE  SfinOFItiRINOVS  PLEV&ITIS  503 

method,  formulated  a  classification  of  pleural  diseases,  based  on  the 
varying  proportion  of  different  cells  in  pleural  fluids,  and  suggested  the 
term  "cytodiagnosis."  Widal  stated  that  (f)  a  predominance  of 
polynuclear  leukocytes  means  an  effusion  of  infectious  origin  (pneu- 
mococcus,  streptococcus,  staphylococcus);  (2)  of  lymphocytes,  a 
tuberculous  effusion;  and  (3)  of  endothelial  cells,  especially  if  in 
plaques  or  sheets,  an  effusion  of  mechanical  origin. 

More  recent  observations  make  it  probable  that  the  character  of 
the  cells  in  pleural  fluids  depends  not  only  on  the  cause  of  the  process, 
but  also  on  the  intensity  of  the  pleural  reaction.  The  predominance 
of  one  type  of  cell,  therefore,  cannot  be  regarded  as  a  specific  indica- 
tion of  an  infectious,  tuberculous,  or  mechanical  origin,  although 
Widal's  formulae  have  been  sufficiently  verified  to  warrant  a  probable 
diagnosis,  provided  the  clinical  character  of  the  case  accords  with  the 
microscopic  findings.  The  method  is  thus  a  valuable  accessory  in  diag- 
nosis, but  must  not  be  expected  to  establish  the  diagnosis  of  itself  alone. 

Various  exceptions  to  the  above  formulae  must  be  noted.  They 
limit  the  diagnostic  value  of  the  procedure.  An  excess  of  polynuclear 
leukocytes  in  infectious  pleuritis  is  subject  to  least  variation.  Con- 
cerning the  lymphocytosis  of  pleural  tuberculosis,  it  should  be  noted 
that  a  transient  excess  of  polynuclear  neutrophils  has  been  found  by 
Widal  and  others  in  its  early  stages.  The  secondary  infection  of  a 
pleura  already  the  site  of  tuberculosis  may  likewise  modify  the  char- 
acter of  the  cellular  elements,  with  an  increase  in  the  relative  propor- 
tion of  polynuclear  cells.  In  regard  to  the  predominance  of  endothelial 
cells  in  mechanical  effusions,  it  has  been  noted  that  they  are  relatively 
most  numerous  in  the  early  stages  of  the  disease.  In  long-standing 
transudates,  Naunyn1  has  shown  that  the  proportion  of  endothelial 
cells  may  diminish  and  lymphocytes  may  be  in  excess.  Lymphocy- 
tosis has  been  present  without  a  reaction  to  tuberculin  and  in  transu- 
dates shown  by  autopsy  not  to  be  tuberculous.  As  in  fluids  with 
lymphocytosis,  so,  also,  in  those  with  an  excess  of  endothelial  cells, 
an  infection  may  raise  the  number  of  polynuclear  cells. 

In  malignant  disease  of  the  pleura,  the  cellular  elements  conform 
more  nearly  to  those  found  in  mechanical  effusions,  with  an  excess 
of  endothelial  cells,  but  large  numbers  of  spindle  cells  may  suggest 
sarcoma,  as  in  Warthin's  case.  Examination  of  the  fluid  in  conjunc- 
tion with  the  history  and  physical  examination  may  confirm  an 
otherwise  doubtful  diagnosis. 

In  experiments  on  animals,  a  lymphocytic  pleuritis  has  been  pro- 
duced by  the  injection  of  diphtheria  bacilli  and  diptheria  toxin.  The 
bearing  of  such  experiments  on  cytodiagnosis  is  still  an.  open  question. 

3.  Bacteriology. — For  the  demonstration  of  the  pneumococcus,  the 
pyogenic  cocci,  and  other  organisms  capable  of  cultivation,  smear 
preparations  should  be  made  and  suitable  media  inoculated. 

1  Deut.  med.  Woch.,  1903,  18  V.  B.,  p  140. 


504  DISEASES  of  THE  PLEURA 

Tubercle  Bacillus. — Special  methods,  the  results  of  which  have 
already  been  mentioned  under  Etiology,  have  been  devised  for  its 
demonstration. 

Inoscopy. — Jousset,1  in  1903,  proposed  a  simple  method  for  the 
demonstration  of  tubercle  bacilli  in  coagulable  fluids.  After  with- 
drawal, the  fluid,  at  least  100  c.c.  in  amount,  is  allowed  to  clot.  The 
clot  is  removed  and  washed  free  of  serum  on  sterile  gauze,  with  sterile 
water,  then  placed  in  a  flask  containing  10  to  30  c.c.  of  the  following 
digesting  fluid:  Pepsin,  1  to  2  grams,  pure  gylcerin  and  strong  hydro- 
chloric acid  of  each  10  c.c,  sodium  fluorid  3  grams,  and  distilled  water 
to  1000  c.c.  The  flask  is  placed  in  the  incubator  at  38°  C.  until  the 
clot  is  digested.  Two  to  three  hours  are  usually  needed.  Frequent 
agitation  of  the  fluid  hastens  the  process.  The  digested  fluid  is  sedi- 
mented,  the  supernatant  fluid  decanted,  and  from  the  precipitated 
material  smears  are  made  with  the  platinum  loop.  These  are  dried 
and  stained  for  tubercle  bacilli. 

Sedimentation^ — Zebrowski2  takes  at  least  100  c.c.  of  fluid,  adds 
an  equal  volume  of  1  per  cent,  sodium  flourid  to  prevent  coagulation, 
and  allows  the  solution  to  stand  in  a  cool  place  for  twenty-four  hours. 
The  supernatant  fluid  is  decanted  and  the  precipitate  centrifugalized. 
Smears  made  from  the  material  thus  obtained  are  investigated  for 
tubercle  bacilli,  as  already  described.  The  greatest  care  should  be 
taken  that  bacilli  in  fluids  previously  examined  are  not  left  clinging 
to  the  apparatus. 

Animal  Inoculation. — All  instruments  must  be  sterilized.  Intra- 
peritoneal inoculation  of  guinea-pigs  is  most  successful.  For  the 
demonstration  of  tubercle  bacilli,  large  amounts  of  fluid  must  be 
injected,  but  in  divided  doses.  If  the  animal  lives,  three  months 
should  be  allowed  to  elapse  before  the  examination  is  made.  Le  Dam- 
any3  made  injections  each  week  of  10  to  50  c.c.  of  fluid,  varying  the 
amount  according  to  the  toxicity  of  the  fluid,  and  was  thus  able  to 
inoculate  as  much  as  300  c.c.  The  fluid  was  preserved  in  test  tubes 
of  small  caliber,  then  transferred  to  a  medium-sized  tube,  open  at 
both  ends,  one  of  which  was  drawn  to  a  blunt  extremity  and  inserted 
through  a  small  abdominal  incision.  Escape  of  fluid  about  the  incision 
was  prevented  by  a  U-shaped  suture.  If  the  fluid  failed  to  flow,  the 
free  end  of  the  tube  was  plugged  with  cotton  and  carefully  heated,  thus 
insufflating  the  contents.  In  this  way  both  clot  and  sediment  were 
inoculated. 

Prognosis. — In  general,  the  immediate  prospect  in  serofibrinous 
pleuritis  is  good.  Large  or  double  effusions  may,  however,  be  suddenly 
fatal.  Of  500  cases  in  the  writer's  series,  4  (0.8  per  cent.)  died  without 
other  obvious  cause  than  the  effusion.  In  one,  large  amounts  of  fluid 
rapidly  reaccumulated,  conforming  to  the  uncommon  variety  known 
as  pleuritis  acutissima.    No  autopsy  was  obtained.    The  three  remain- 

1  La  semaine  med.,  1903,  p.  22.  2  Deut.  med.  Woch.,  1905,  Nr.  36. 

3  La  presse  med.,  November  24,  1897,  p.  329. 


ACUTE  .SEROFIBRINOUS  PLEURITIC  505 

ing  patients  were  not  tapped.  Two  had  double  effusions,  in  one  of 
whom  autopsy  showed  that  death  was  due  to  pulmonary  embolism; 
in  the  second  no  other  cause  of  death  was  found  postmortem  than 
edema  of  the  lungs.  In  the  last  patient  there  was  a  large  unilateral 
accumulation,  and  examination  after  death  showed  pulmonary  embo- 
lism. Thoracentesis  might  have  been  life  saving  in  these  cases.  If 
an  infectious  and  non-tuberculous  cause  can  be  established,  the  prog- 
nosis is  favorable. 

Prophylaxis. — In  a  large  majority  of  the  cases  this  embraces 
measures  for  the  prevention  of  infection  with  the  tubercle  bacillus 
and  other  organisms. 

Treatment. — 1.  The  Natural  or  Spontaneous  Cure. — The  large 
proportion  of  cases  coming  to  autopsy  with  pleural  adhesions,  asso- 
ciated with  fibrocaseous  or  calcined  pulmonary  lesions,  shows  that 
pleural  disease,  directly  or  indirectly  dependent  on  the  tubercle  bacillus, 
is  frequently  arrested  or  healed.  Tuberculous  nodules  in  the  pleura, 
as  elsewhere,  may  be  walled  off  by  a  dense  envelope  of  fibrous  tissue, 
and  thus  prove  of  little  danger  to  the  individual,  forming  latent  foci. 
Calcification  may  take  place,  as  in  5  of  27  cases  (M.  G.  H.),  with 
obsolete  tuberculosis  as  a  result.  Tuberculous  granulations  in  a 
part  or  the  whole  of  the  pleura  may  finally  be  converted  into  firm, 
fibrous  tissue,  ending  in  obliteration  of  the  pleural  sac  and  no  further 
trouble  from  the  process.  The  clinical  history  of  cases  of  certain  or 
probable  pleural  tuberculosis  shows  that  recovery  is  not  infrequent. 

2.  General  Measures. — For  purposes  of  treatment,  it  is  best  to 
assume  every  case  of  primary  serofibrinous  pleurisy  to  be  tuberculous, 
unless  there  is  good  reason  to  believe  otherwise.  Fortunately,  many 
patients  are  still  in  fair  health  when  they  first  come  under  observa- 
tion. The  course  of  the  disease  is  often  slow  and  spontaneous  recovery 
frequent,  which,  indeed,  too  often  fosters  half-way  measures  in  its 
care.  As  in  tuberculosis  elsewhere,  we  must  rely  chiefly  on  rest,  fresh 
air,  and  the  improvement  of  nutrition.  It  must  be  constantly  in 
mind  that  the  pleural  disease  is  usually  secondary  to  tuberculosis  of 
the  lung  or  thoracic  glands,  as  is  shown  by  autopsy,  although  the 
primary  focus  often  escapes  detection  during  life. 

If  we  are  to  secure  the  hearty  cooperation  of  the  patient,  he  should 
be  frankly  told  the  seriousness  of  his  condition.  We  can  otherwise 
hardly  secure  his  acceptance  of  the  necessary  restrictions  on  his  mode 
of  life.  The  chances  with  primary  serofibrinous  effusion  are  about 
3  or  4  in  10  that  pulmonary  or  other  tuberculosis  will  appear  within  a 
period  of  six  or  seven  years.  These  figures  have  this  hopeful  aspect, 
however,  that  they  are  for  the  most  part  gathered  from  cases  in  which 
treatment  terminated  with  the  disappearance  of  the  effusion.  They 
probably,  therefore,  represent  the  natural  evolution  of  the  disease, 
and  a  longer  or  even  a  permanent  arrest  may  be  expected  in  patients 
who  can  and  will  consent  to  more  careful  supervision  and  regulation 
of  the  daily  life. 


506  DISEASES  OF   THE  I'LEIh'A 

During  the  acute  stage,  while  there  is  fever,  rest  in  bed  should  be 
enforced  and  maintained  until  the  temperature  is  normal.  After  the 
acute  symptoms  have  subsided,  the  patient  may  cautiously  be  given 
greater  liberty,  careful  watch  being  kept  meanwhile  on  the  tempera- 
ture. The  supply  of  fresh  air  should  be  continuous  and  abundant,  by 
night  as  well  as  by  day.  Means  similar  to  those  in  pulmonary  tuber- 
culosis may  be  taken  to  secure  this.  In  undernourished  individuals 
an  increase  in  weight  should  be  sought  from  the  beginning  and  for 
such  patients  extra  feeding  must  be  employed.  The  food  should  be 
simple  and  nutritious  and  extra  feedings  of  milk  or  eggs  may  be  given 
between  the  regular  meals.  Fat  is  important  and  is  best  given  in  the 
form  of  cream  or  fresh  butter. 

The  treatment  should  not  end  with  the  subsidence  of  fever  and  the 
disappearance  of  fluid.  Patients  who  have  apparently  recovered 
should  be  kept  under  observation,  and  every  effort  made  to  maintain 
the  general  condition  at  a  high  level.  Country  is  better  than  city  life. 
The  occupation  should  be  carefully  chosen.  Overcrowded,  dusty,  or 
badly  ventilated  places  should  be  avoided.  Indiscretion  and  neglect 
may  bring  the  patient  under  observation  a  second  time  with  pul- 
monary or  other  tuberculosis  too  late  for  successful  treatment.  Loss 
of  weight,  fever,  cough,  or  other  suspicious  symptoms  should  receive 
immediate  attention,  and,  if  necessary,  a  further  course  of  rest,  out- 
door life,  and  extra  feeding. 

3.  Local  Applications. — These  are  for  the  alleviation  of  symptoms. 
The  ice-bag,  hot-water  bottle,  and  hot  applications  repeated  every 
two  hours  may  efficiently  relieve  pain,  for  which,  however,  morphin 
may  be  necessary.  It  is  doubtful  if  blisters  have  other  than  a  harmful 
effect,  making  the  patient  uncomfortable  and  adding  to  the  danger 
of  thoracentesis,  if  the  skin  becomes  infected.  Strapping  the  affected 
side  only  further  displaces  the  lung  and  other  organs.  It  may  actually 
hinder  absorption  by  compressing  the  lymph  channels. 

4.  Special  Measures.  —  Thoracentesis.  —  Indications.  —  In  general, 
the  opinion  of  the  present  time  is  in  favor  of  tapping  serofibrinous 
effusions  (1)  with  pressure  symptoms,  such  as  severe  dyspnea,  cya- 
nosis, or  rapidly  developing  cardiac  weakness;  (2)  of  large  amount, 
with  dislocation  of  heart  and  mediastinum,  even  without  pressure 
symptoms;  and  (3)  of  medium  amount  when  other  means  have  failed 
to  bring  about  absorption  and  two  or  three  weeks  have  elapsed. 

With  pressure  symptoms  and  large  effusions,  thoracentesis  is  impera- 
tive and  should  be  done  without  delay.  It  has  been  the  unfortunate 
experience  of  many  physicians  to  decide  on  evacuation  in  such  cases 
within  a  given  time,  before  the  expiration  of  which  the  patient  has 
suddenly  died.  The  presence  of  fever  is  not  a  contra-indication. 
Left-sided  effusions  are  somewrhat  more  dangerous.  Bilateral  fluid, 
of  only  medium  amount,  should  likewise  be  immediately  evacuated. 
The  removal  of  medium  and  small  effusions  is  not  immediately  neces- 
sary and  a  short  delay  may  promote  repair  or  furnish  evidence  of 


ACUTE  SEROFIBRINOUS  PLEURITIS  507 

spontaneous  absorption.  It  is  customary  to  wait  two  to  three  weeks, 
but  earlier  removal  may  well  be  considered.  Jt  alleviates  symptoms 
from  pressure  and  may  prevent  the  formation  of  venous  thrombi  and 
the  danger  of  pulmonary  infarction.  The  withdrawal  of  fibrinous 
material,  hindering  absorption,  may  shorten  the  course  of  the  disease. 
The  danger  of  adhesions,  permanent  fixation  of  the  lung  in  an  abnor- 
mal position  and  persistent  reaccumulation  of  fluid  increases  with  the 
duration  of  the  effusion. 

Selection  of  Cases  for  Tapping. — The  character  of  the  fluid  is  impor- 
tant in  the  decision  between  thoracentesis  and  thoracotomy.  With 
clear  fluid,  thoracentesis  is  the  operation  of  choice.  Open  incision 
is  followed  by  suppuration,  which  is  to  be  avoided.  With  turbid 
fluids  the  decision  is  more  difficult.  They  are  on  the  border  line  between 
serofibrinous  and  purulent  effusion.  Of  27  cases  in  the  writer's  series 
with  turbid  fluid  containing  an  excess  of  polynuclear  cells,  15  were 
cured  by  thoracentesis  alone.  In  12,  pus  was  found  at  later  tapping 
and  thoracotomy  was  performed.  The  tendency  of  pleural  fluid  to 
sediment  within  the  chest  must  be  remembered.  A  sample  from  the 
upper  layer  may  be  turbid,  while  pus  may  exist  below.  Turbid  fluids 
secondary  to  lobar  pneumonia  or  due  to  the  pneumococcus  are  rela- 
tively favorable  for  thoracentesis.  With  merely  an  excess  of  poly- 
nuclear cells  in  the  differential  count,  tapping  alone  may  be  considered. 
Pneumococci  may  be  found  in  such  exudates,  but  are  often  incapable 
of  cultivation.  With  abundant  or  necrotic  leukocytes  and  pneumococci 
on  cultivation,  operation  is  usually  necessary.  Streptococcus  infections 
are  usually  purulent,  or  rapidly  become  so,  and  generally  demand 
open  incision.  The  general  symptoms,  the  amount  of  fluid  and  rapidity 
of  reaccumulation  must  also  be  considered. 

Apparatus. —  Needle  or  Trocar? — The  needle  is  simple  and  less 
expensive,  but  has  two  drawbacks.  Its  unprotected  point  may  wound 
the  expanding  lung  or  the  diaphragm.  More  important  than  this, 
however,  a  bit  of  tissue  punched  out  during  insertion  or  a  small  mass 
of  fibrin  may  effectually  occlude  its  lumen.  To  dislodge  such  particles, 
the  needle  must  be  withdrawn,  if  the  danger  of  pneumothorax  and 
possible  infection  of  the  pleura  are  to  be  avoided.  Kronig1  has  devised 
a  satisfactory  needle,  the  point  of  which  is  rendered  harmless  by 
thrusting  foreward  an  enclosed  and  blunt-pointed  cannula.  The  trocar 
with  lateral  outlet  presents  a  harmless,  blunt  end  after  the  removal  of 
the  stylet  and  can  be  thrust  farther  in,  elevated  or  depressed  without 
danger  to  neighboring  structures.  If  plugged,  the  obstruction  is 
readily  removed  by  the  insertion  of  the  stylet  and  without  danger 
of  pneumothorax,  if  the  packing  is  tight,  as  it  should  be,  about  the 
stylet.  A  negative  puncture  with  an  ordinary  needle  is  less  reliable 
than  with  the  trocar. 

Various  trocars  have  been   devised.     The  cannula  should   be  at 

1  Med.  Klinik.,  Berlin,  1906,  ii,  131-135. 


-,I)S 


DISEASES  OF   THE   PLEURA 


least  7  cm.  long.  In  general,  the  internal  diameter  should  not 
exceed  1 .")  to  2  nun.  It  is  advantageous  to  have  several  sizes  at 
hand.  The  stylet  should  fit  tightly  at  the  extremity  of  the  cannula, 
which  should  taper  gradually  to  a  thin  edge  to  avoid  difficulty 
and  pain  in  Us  introduction.  A  lateral  outlet  is  needed  for  thoracic 
puncture,  in  order  that  the  stylet  may  be  moved  in  and  out  without 
disturbing  the  connections.     A  stop-cock  on  the  lateral  outlet  is  useful. 

Fig.  SO 


Vfter  Hoppc-Soylor.) 


Toward  the  proximal  end  of  the  instrument  and  this  side  of  the  lateral 
outlet  there  should  be  a  stop-cock,  to  guard  against  leakage  of  air 
about  the  entrance  of  the  stylet  and  to  maintain  the  instrument  air- 
tight if  the  latter  is  removed.  The  stylet  should  run  through  a  com- 
partment capable  of  air-tight  connection  with  the  instrument,  and 
the  play  of  the  stylet  through  this  compartment  should  also  be  air- 
tight in  order  that  it  may  be  moved  in  and  out  without  danger  of 
producing  pneumothorax.  The  proximal  end  carrying  the  stylet 
is  the  weak  part  of  the  apparatus,  since  it  is  difficult  to  secure  an  air- 
tight all-metal  connection  without  making  the  instrument  too  cumber- 


ACUTE  SEROFIBRINOUS  PLEURITIS 


509 


some  and  without  the  use  of  oil.  The  introduction  of  rubber  washers, 
although  they  need  to  be  frequently  changed,  is  the  most  satisfactory 
solution.  The  writer  uses  an  air-tight  trocar,1  constructed  on  the 
principles  mentioned,  with  stop-cock  on  lateral  outlet  and  cannula. 

(Figs.  87  and  88.) 

Fig.  87  Fig.  88 


Air-tight  trocar  for  thoracentesis. 

Methods. — In  general,  there  are  only  two  safe  and  reliable  methods, 
i.  e.,  siphonage  and  aspiration. 

1.  Siphonage. — This  is  readily  carried  out.  A  trocar  such  as  that 
described  above  or  Kronig's  needle  may  be  used.  A  rubber  tube 
about  75  cm.  long,  a  clamp  for  the  tube,  a  glass  funnel,  sterile  water 
or  salt  solution  are  also  needed.  If  the  trocar  is  used,  one  end  of  the 
tube  is  fastened  to  its  lateral  outlet,  the  other  to  the  glass  funnel, 
by  means  of  which  the  apparatus  is  filled  with  the  sterile  solution. 
When  the  instrument  is  full,  escape  of  the  solution  is  prevented  by 
fastening  the  clamp  on  the  rubber  tube  or  closing  the  stop-cock  on 
the  lateral  outlet.  The  tube  now  contains  a  column  of  water,  which, 
on  the  release  of  the  clamp  or  stop-cock,  is  capable  of  exerting  sufficient 

1  An  air-tight  trocar  for  thoracentesis,  Jour.  Amer.  Med.  Assoc,  1908. 


510 


DISEASES  OF  THE  PLEURA 


aspiratory  force  to  overcome  a  negative  pressure  in  the  thorax  under 
any  ordinary  conditions.  The  trocar  is  inserted  into  the  chest  while 
the  free  end  of  the  rubber  tube  is  held  beneath  the  surface  of  the 
sterile  solution,  thus  preventing  aspiration  of  air,  provided  the  negative 
pressure  within  the  chest  should  be  greater  than  the  weight  of  the 
column  of  water  in  the  rubber  tube.  By  this  method  there  is  no  danger 
of  an  excess  of  negative  pressure,  which  may  be  varied  at  will  by 
simple  elevation  and  depression  of  the  free  end  of  the  tube.  Kronig 
attaches  the  free  end  of  the  rubber  tube  to  a  glass  tube  passing  nearly 
to  the  bottom  of  a  flask  partly  filled  with  sterile  solution,  and  with 
a  curved  outlet  at  the  top  (Fig.  89).  There  is  no  danger  of  the  entrance 
of  air  or  of  reflux  of  contaminated  fluid.  The  pressure  of  the  pleural 
fluid  may  be  measured  by  elevation  and  depression  of  the  flask,  noting 
the  difference  between  its  upper  level  in  the  flask  and  the  chest,  when 
equilibrium  is  established. 

Fig.  89 


Kronig's  method. 

2.  Aspiration. — The  most  satisfactory  method  is  by  means  of  a 
bottle,  connected  on  the  one  hand  with  the  chest  and  on  the  other 
with  an  aspirator  by  means  of  rubber  tubing.  Aspiration  may  be 
effected  by  means  of  a  pump,  as  in  Potain's  method.  A  rubber  bulb 
may  be  used,  as  in  Alexander's1  modification  of  Unverricht's  method. 
Furbringer2  secures  negative  pressure  in  the  bottle  by  aspiration  with 
the  mouth,  which  can  hardly  be  recommended.  In  Dieulafoy's  rack 
aspirator3  the  evacuated  fluid  flows  directly  into  the  vacuum  apparatus. 

1  Dcut.  mcd.  Woeh.,  1893,  Nr.  10,  S.  241. 

2  Berl.  klin.  Woch.,  1888,  Nr.  13,  S.  254. 

3  A  Treatise  on  Pneumatic  Aspiration,  London,  1873. 


ACUTE  SEROFIBRINOUS  PLEURITIS 


511 


Stinzing1  recommends  a  tall,  graduated  flask  for  the  reception  of  the 
fluid.  In  both  Stinzing's  and  Frankel's2  articles  a  full  description  and 
discussion  of  various  instruments  will  be  found. 


Fig.  90 


Aspiration  with  Potain's  apparatus.     (After  Hoppe-Seyler.) 

Potain's  apparatus  is  in  most  general  use.  The  pump  is  capable 
of  a  dangerous  degree  of  aspiratory  force.  Only  sufficient  aspiration 
should  be  used  to  just  maintain  the  flow.  The  rubber  tubing  should 
be  thick  and  all  connections  must  be  air-tight.  A  piece  of  glass  tubing 
inserted  between  the  trocar  and  bottle  will  be  of  assistance  in  noting 
the  result  of  aspiration.  If  desired,  a  mercury  manometer  may  readily 
be  connected  with  the  bottle,  thus  measuring  the  negative  force.  An 
extension  of  the  inlet  to  the  bottom  of  the  bottle  will  prevent  any 
back  flow  of  air,  provided  the  negative  pressure  within  the  thorax 
becomes  greater  than  within  the  bottle.  As  a  receptacle  for  the  fluid 
a  bottle  of  the  proper  size  to  fit  the  rubber  stopper,  graduated  at 
different  levels  by  marks  of  a  file  and  capable  of  holding  from  1500  to 
2000  c.c,  should  be  chosen.  The  glass  should  be  of  such  a  quality  as 
to  stand  sterilization  without  breaking. 

1  Handbuch  der  Therapie  innerer  Krankheiten,  1902,  Bd.  iii. 

2  Handbuch  der  physikalischen  Therapie,  Theil  ii,  Bd.  i,  Goldscheider  und  Jacob, 
1902. 


512  DISEASES  OF    THE   PLEURA 

Technic.—The  instruments  should  be  sterilized  just  before  use.  The 
trocars,  all  rubber  tubing,  rubber  stopper  to  the  bottle,  scissors,  and 
hypodermic  syringe,  it'  this  is  used,  should  be  boiled.  Disinfection 
with  antiseptics  is  uncertain,  and  may  interfere  with  subsequent 
bacteriologic  tests  of  the  fluid.  The  operator's  hands  should  be 
scrubbed  clean  and  disinfected  with  alcohol.  The  patient's  side 
should  be  prepared  over  a  wide  area  with  soap  and  water,  using  a 
piece  of  sterile  gauze  in  place  of  a  brush.  It  is  then  dried  with  sterile 
gauze  and  disinfected  writh  alcohol.  If  operation  is  not  at  once  under- 
taken, a  pad  of  sterile  gauze  should  be  applied.  The  apparatus  should 
be  set  up,  tested  by  the  aspiration  of  sterile  water,  and  the  air  in  the 
bottle  should  be  under  negative  pressure  before  the  puncture  is  made. 
The  site  chosen  for  puncture  will  vary  with  the  amount  and  position 
of  the  effusion.  The  position  of  the  heart  must  be  known.  An  encap- 
sulated exudate  must  be  sought  with  due  regard  to  anatomical  land- 
marks. With  large  or  medium  and  free  effusions,  the  puncture  may 
be  made  in  the  fifth  or  sixth  intercostal  space  in  the  midaxilla,  with 
small  effusions  in  the  seventh  space  between  the  scapular  and  posterior 
axillary  lines.  The  choice  of  the  latter  situation  has  certain  advantages, 
in  that  the  patient  is  not  disturbed  by  seeing  the  procedure  and  the 
trocar  will  be  nearer  the  lower  level  of  the  fluid.  As  the  dome  of  the 
diaphragm  rises  normally  as  high  as  the  fourth  interspace  in  the  nipple 
line,  the  sixth  rib  in  the  midaxilla  and  the  eighth  rib  in  the  scapular 
line,  a  lower  level  cannot  safely  be  chosen.  In  fresh  effusions,  the  lung, 
the  heart,  and  the  diaphragm  are  displaced  away  from  the  selected 
site,  and  there  is  little  danger  of  their  injury,  but  with  chronic  cases, 
with  narrowing  of  the  interspaces,  contraction  of  the  side  and  elevation 
of  the  diaphragm,  a  higher  level  should  be  selected.  The  interspaces 
should  be  carefully  counted  before  the  operation  is  undertaken.  A 
thickness  of  2  to  4  cm.  or  more  under  ordinary  conditions  must  be 
allowed  for  the  thoracic  wall.  In  fat  subjects,  or  in  the  presence  of 
a  thick  layer  of  fibrin,  the  trocar  may  fail  to  find  fluid  even  at  this 
distance.  The  patient  is  best  placed  on  the  bed  to  avoid  unnecessary 
exertion  after  the  operation.  The  puncture  may  be  made  with  the 
patient  in  the  sitting  position  or  reclining  on  the  affected  side.  The 
intercostal  spaces  may  be  widened  by  placing  the  hand  of  the  affected 
side  on  the  opposite  shoulder.  Local  anesthesia,  as  for  exploratory 
puncture  (see  p.  498),  should  precede  the  operation.  The  subcutaneous 
injection  of  morphin  has  been  advised,  but  may  inhibit  symptoms 
which  would  otherwise  warn  the  operator  of  approaching  danger. 

As  a  guide  for  the  introduction  of  the  trocar,  the  selected  interspace 
is  palpated  by  the  fingers  of  one  hand,  while  in  the  other  the  trocar 
is  held  with  the  blunt  end  of  the  stylet  firmly  against  the  palm  and  the 
end  of  the  index  finger  about  4  cm.  from  the  point,  thus  guarding 
against  too  deep  an  initial  puncture.  The  instrument  is  slowly  and 
carefully  introduced,  perpendicular  to  the  surface,  just  above  the 
rib,  to  avoid  the  intercostal  artery.     It  is  pushed  in  until  from  the 


ACUTE  SEROFIBRINOUS  PLEURITIS  513 

lack  of  further  resistance  the  operator  may  judge  that  the  point  has 
reached  fluid.1  Insertion  during  forced  inspiration  may  depress  the 
diaphragm  out  of  danger  when  a  low  site  is  chosen.  Preceding  with- 
drawal, the  operator  may  conveniently  appose  a  piece  of  sterile  gauze, 
inclosing  the  trocar,  firmly  against  the  region  of  puncture.  The 
cannula  should  be  quickly  withdrawn.  Rarely  pleural  fluid  may 
continue  to  flow  from  the  wound.  Slight  bleeding  from  the  injury 
of  small  bloodvessels  may  occur.  Pressure  usually  suffices  to  stop  this, 
but,  if  necessary,  a  stitch  may  be  taken  through  the  wound.  A  dress- 
ing may  be  made  from  a  small  pad  of  sterile  gauze  cut  to  an  appropri- 
ate size  and  held  in  place  by  adhesive  plaster  or  collodion. 

The  trocar  and  rubber  tubing  should  be  cleaned  at  once  after  the 
operation.  This  is  conveniently  done  by  running  first  cold  water, 
then  alcohol,  and  finally  ether  through  the  apparatus,  which  should 
be  dry  when  put  away. 

Symptoms  and  Difficulties  during  Evacuation. — Faintness  and 
vertigo  are  not  uncommon,  and  are  usually  due  to  psychic  disturb- 
ance. They  may  be  relieved  by  placing  the  patient  in  the  reclining 
position.  An  occasional  slight  cough  is  frequent  toward  the  end  of 
the  evacuation.  If  severe,  the  operation  should  be  stopped.  Cough 
may  be  due  to  pleural  irritation,  to  hyperemia,  or  edema  of  the 
expanding  lung.  If  it  persists,  morphin  may  be  given.  Blood  may 
rarely  be  expectorated  during  evacuation.  It  may  arise  from  the 
rupture  of  small  bloodvessels  in  the  lung,  from  congestion,  or  from 
puncture  of  the  lung  with  the  trocar,  and  when  it  occurs  it  is  best  to 
discontinue  the  operation.  Pain  is  not  common,  but,  if  severe,  is  a 
contra-indication  to  continuance,  as  it  may  indicate  undue  tension 
on  pleural  adhesions.  There  may  be  a  feeling  of  dyspnea  and  general 
discomfort,  perhaps  cardiac  in  origin,  and  severe  enough  to  warrant 
a  halt  in  the  operation. 

The  operator  may  have  difficulty  in  inserting  the  trocar  between 
narrow  interspaces  and  a  smaller  instrument  may  be  necessary. 
Unexpected  movement  on  the  part  of  the  patient  may  direct  the 
point  of  the  trocar  against  a  rib.  After  introduction  and  the  with- 
drawal of  the  stylet,  no  fluid  may  follow.  A  bit  of  fibrin  may  have 
closed  the  opening,  or  if,  after  reintroduction  of  the  stylet,  the  punc- 
ture is  still  negative,  the  trocar  may  need  to  be  inserted  farther,  in 
a  different  direction,  or  partially  withdrawn.  The  presence  of  firm 
tissue  in  the  track  of  the  instrument  can  usually  be  appreciated  as 
a  resistance  against  forward  or  lateral  motion.  Introduction  else- 
where may  be  more  successful.  Finally,  there  may  be  no  fluid,  but 
negative  punctures  never  positively  exclude  it.     Interruption  of  the 

1  It  is  convenient  to  know  that  at  the  level  of  junction  of  the  third  costal  cartilage 
with  the  sternum  (sixth  dorsal  vertebra),  the  distance  from  the  skin  to  the  bloodvessels 
at  the  root  of  the  lung  in  an  average  adult  male  was  found  by  Piersol  (Musser,  Jour. 
Amer.  Med.  Assoc,  January  5,  1907)  to  be  7  cm.  in  the  midaxillary  line  on  the  left  side 
and  at  a  greater  depth  in  other  regions  of  the  same  transverse  section. 
33 


514  DISEASES  OF   THE  PLEURA 

flow  during  evacuation  may  be  due  to  fibrin,  apposition  of  lung 
or  diaphragm  against  the  end  of  the  cannula,  or  equalization  of 
pressure  within  and  outside  the  chest.  The  last  may  happen  even 
with  considerable  fluid  remaining,  provided  the  lung  is  firmly  bound 
down  in  a  retraeted  position. 

Amount  of  Fluid  to  be  Withdrawn. — This  depends  on  the  size  of  the 
effusion.  Absorption  may  follow  removal  of  very  small  quantities. 
The  rare  occurrence  of  serious  symptoms,  and  even  of  death,  follow- 
ing the  evacuation  of  large  amounts  of  fluid  is  a  warning  not  to  be 
safely  disregarded.  With  large  effusions,  as  much  as  1500  c.c.  may 
be  withdrawn,  provided  no  unfavorable  symptoms  arise  during  the 
proeess.  Much  larger  quantities  are  often  removed  without  an  un- 
favorable result,  and  with  very  large  effusions,  in  which  the  fluid 
runs  without  aspiration  or  symptoms,  as  much  as  2000  c.c.  may  be 
evacuated.  If  danger  is  to  be  avoided,  however,  this  amount  should 
only  rarely  be  reached  and  never  exceeded.  The  remaining  fluid  will 
probably  be  absorbed;  if  not,  the  procedure  can  be  repeated.  With 
small  effusions  it  is  unnecessary  to  evacuate  the  last  drop.  Small 
amounts  of  fluid  remaining  are  usually  readily  absorbed.  The  longer 
the  effusion  has  lasted  and  the  older  the  patient,  the  smaller  the 
amount  of  fluid  which  can  be  safely  withdrawn.  More  abundant 
adhesions  and  less  elastic  lung  then  increase  the  danger.  In  the 
presence  of  pulmonary  tuberculosis,  especial  care  should  be  exercised 
in  the  removal  of  fluid  to  avoid  rupture  of  adhesions  and  artificial 
pneumothorax. 

Duration  of  the  Operation. — It  is  safer  to  evacuate  fluid  slowly. 
A  half-hour  may  be  consumed  in  the  removal  of  1500  c.c.  in  order 
that  neighboring  structures  may  gradually  readjust  themselves. 

Injections. — The  replacement  of  the  evacuated  fluid  by  air  has 
been  recommended.  Filtered  air,  oxygen,  and  sterile  salt  solution 
have  more  recently  been  used.  Air  is  said  to  be  of  advantage  in  the 
rare  chronic  cases  in  which  adhesions  prevent  reexpansion  of  the  lung 
following  evacuation,  or  with  bloody  fluids  in  which  negative  pleural 
pressure  only  leads  to  renewed  hemorrhage.  Absorption  of  the  air 
takes  place  slowly.  Barr1  replaces  the  evacuated  fluid  by  about  two- 
thirds  to  three-fourths  of  the  original  volume  with  filtered  air,  and 
finally  injects  4  to  8  c.c.  of  a  solution  of  adrenalin  hydrochloride  (1  to 
1000).  Injections  of  air  may  favor  fixation  of  the  lung  in  an  abnormal 
position  by  delaying  reexpansion.  Infection  from  organisms  present 
in  the  air  is  a  possible  danger. 

Repetition  of  Tapping. — One  tapping  suffices  in  about  75  per  cent, 
of  the  cases.  In  about  20  per  cent,  of  the  remaining  cases  there  is  no 
more  fluid  after  the  second  operation.  In  some  cases  evacuation 
must  be  frequently  repeated.  It  is  often  difficult  to  determine  the 
presence  of  fluid  in  cases  which  have  been  tapped,  owing  to  the  changes 

1  British  Med.  Jour.,  1904,  p.  1003. 


ACUTE  SEROFIBRINOUS  PLEUBITIS  515 

in  the  pleura.  Percussion  often  gives  dubious  results  and  more  reliance 
may  be  placed  on  the  absence  of  tactile  fremitus,  the  respiratory 
murmur,  and  cardiac  displacement. 

Dangers  of  Thoracentesis. — There  is  some  danger  in  the  perform- 
ance of  thoracentesis.  This  is  reduced  to  a  minimum  by  the  strictest 
asepsis,  the  use  of  an  air-tight  trocar,  rather  than  an  ordinary  needle, 
the  slow  withdrawal  of  only  moderate  amounts  of  fluid  without 
forcible  aspiration,  and  a  careful  selection  of  cases.  Unavoidable 
accidents  are  extremely  rare.  Patients  are  more  often  sacrificed  by 
hesitation  and  delay  than  by  its  use. 

The  danger  of  converting  a  serous  into  a  purulent  effusion  appears 
to  be  insignificant.  Of  553  tappings  in  my  series,  turbid  fluids 
were  found  in  27,  and  of  these  12  later  became  purulent,  but  the 
suppuration  was  probably  spontaneous.  In  one  instance  a  fluid 
showed  88  per  cent,  of  lymphocytes  at  the  first  tapping  and  78  per 
cent,  polynuclear  cells  when  the  thoracentesis  was  repeated  four 
days  later.  In  a  second  case  a  fluid  at  first  contained  96  per  cent, 
lymphocytes.  The  patient  was  discharged  without  evidence  of 
effusion,  to  return  one  month  later  with  empyema.  Whether  a  simi- 
lar change  would  have  taken  place  without  puncture  is  uncertain. 

Pneumothorax  is  a  more  frequent  result.  In  rare  instances  it  may  be 
due  to  puncture  of  the  lung  or  to  the  rupture  of  adhesions,  pulmonary 
cavities,  or  emphysematous  blebs  during  expansion.  It  is  not  infre- 
quently due  to  the  entrance  of  air  through  an  unguarded  needle  or 
trocar,  as  Sears1  has  emphasized.  It  may  also  result  from  accidental 
inflation  of  the  pleural  sac  with  the  aspirating  pump,  if  the  tubing 
is  misapplied.  Infection  of  the  pleura  may  follow  the  admission 
of  air. 

Subcutaneous  emphysema  may  occur  if  the  lung  is  wounded  and 
air  enters  the  track  of  the  trocar.  It  may  be  local  or  involve  the 
greater  part  of  the  body,  and  is  more  common  after  exploratory  punc- 
ture. Extension  of  malignant  growth  or  tubercle  along  the  track  of 
the  needle  occasionally  occurs.  The  removal  of  pleural  fluid  may 
lead  to  the  detachment  of  thrombi  in  the  heart  or  intrathoracic  vessels, 
with  monoplegia  or  hemiplegia  as  a  result.  Delirium  and  hysterical 
and  epileptic  attacks  have  been  observed.  Urticaria  has  been  noted 
after  thoracentesis,  and  should  always  suggest  echinococcus  disease. 

Albuminous  expectoration  is  of  rare  occurrence.  Terillon2  collected 
21  cases.  Piiesman3  has  reviewed  the  literature  and  reported  an  addi- 
tional instance.  Osier  observed  the  condition  twice  in  195  cases. 
It  occurred  once  in  my  series.  The  albuminous  expectoration 
usually  begins  during  or  shortly  after  the  withdrawal  of  fluid.  Its 
appearance  may  be  delayed,  however,  for  as  long  as  eighteen  hours, 
as  in  Pepper's  case.     It  is   accompanied   by  cough   and  often  by 

1  Amer.  Jour.  Med.  Sci.,  December,  1906,  p.  850. 

2  L'expectoration  albumineuse,  These  de  Paris,  1873. 

3  Amer.  Jour.  Med.  Sci.,  1902. 


51b  DISK  ASKS  OF  THE  PLEURA 

dyspnea,  which  varies  much  in  intensity  and  may  be  extreme, 
with  cyanosis  and  rapid,  feeble  pulse.  Rales  may  be  heard  over  the 
lung  during  the  attack.  Its  duration  and  intensity  are  very  variable. 
It  may  last  for  as  long  as  forty-eight  hours,  and  the  patient  may  die 
of  suffocation.  The  fluid  may  amount  to  as  much  as  a  quart  in  two 
hours,  but  smaller  quantities  are  more  common.  The  expectorated 
fluid  is  serous  and  contains  a  variable  amount  of  blood,  frothy  mucus, 
and  albumin.  In  most  instances  an  excessive  amount  of  fluid  (more 
than  2000  c.c.)  has  been  removed.  The  condition  has  been  more 
often  noted  in  acute  effusions,  but  Riesman's  case  was  chronic. 
In  the  case  in  my  series  only  1000  c.c.  of  fluid  were  withdrawn. 
The  expectoration  began  a  few  minutes  after  the  tapping,  and  lasted 
for  four  hours,  during  which  time  about  500  c.c.  were  expectorated. 
The  pulmonary  symptoms  completely  subsided,  but  the  patient  died 
some  weeks  later,  and  at  autopsy  cirrhosis  of  the  liver  and  associated 
lesions  were  found,  but  no  explanation  of  the  expectoration.  In  fatal 
cases  edema  of  one  or  both  lungs,  cardiac  disease,  fibrinous  plugs 
in  the  bronchi,  and  adherent  pericardium  have  been  found  (Ries- 
man).  The  condition  has  been  ascribed  to  evacuation  of  pleural 
fluid  b}"  way  of  the  bronchi.  This  may  happen  if  the  lung  has  been 
perforated  during  the  puncture.  Spontaneous  rupture  or  filtration 
through  the  lung  has  been  suggested.  It  is  more  probably  due,  how- 
ever to  pulmonary  congestion,  with  edema,  for  which  Riesman  sug- 
gests the  term  "congestion  by  recoil."  It  may  be  conjectured  that 
compression  of  the  lung  is  followed  by  changes  in  its  bloodvessels, 
and  that  in  the  congestion  after  reexpansion  there  is  a  transudation 
of  serum.  Of  51  cases  of  albuminous  expectoration  which  I  have 
reviewed1  13  were  fatal.  A  consideration  of  the  postmortem  reports 
on  14  in  whom  death  immediately  followed  the  operation  or  occurred 
after  an  interval,  suggests  that  pulmonary  inelasticity  from  pleural 
adhesions  or  complicating  cardiac,  pulmonary  or  mediastinal  disease 
is  probably  an  important  contributing  factor. 

Death,  in  rare  instances,  has  followed  even  simple  exploratory 
puncture.  Leichtenstern,2  Russell,3  Sears4  and  others  have  called 
attention  to  the  occurrence  in  rare  instances  of  sudden  death  in  the 
course  of  thoracic  puncture.  Postmortem  examination  of  such  cases 
may  fail  to  disclose  the  cause.  Symptoms  indicating  a  varying  degree 
of  shock  are  not  very  uncommon.  Although  the  cause  cannot  be 
definitely  determined,  yet  the  demonstration  by  Capps  and  Lewis5 
that  in  man  and  in  dogs  irritation  of  an  inflamed  pleura  often  gives 
rise  to  a  reflex  of  cardio-inhibitory  or  vasodilator  type,  with  lowering 
of  the  blood-pressure,  offers  a  suggestive  explanation.    The  inflamed 

1  Lord,  Boston  Med.  and  Surg.  Jour.,  April  15,  1909. 

2  Deut.  Arch.  f.  klin.  Med.,  1879,  vol.  xxv. 

3  St.  Thomas'  Hosp.  Rep.,  London,  1899,  xxviii,  465. 

4  Amer.  Jour.  Med.  Sci.,  December,  1906. 
6  Ibid.,  December,  1907. 


ACUTE  SEROFIBRINOUS  PLEURITIS  517 

pleura  appears  to  be  especially  susceptible,  and  the  nervous  shock 
thus  induced  in  dogs  may  even  be  fatal.  Such  experiments  plainly 
indicate  the  wisdom  of  avoiding  any  unnecessary  play  of  even  a  blunt- 
pointed  cannula  against  the  inflamed  pleura. 

Artificial  pneumothorax  has  occasionally  been  fatal.  Sudden  death 
during  or  after  the  evacuation  of  pleural  fluid  may  be  due  to  embolism. 
Thrombi  in  the  pulmonary  veins  or  the  vense  cavse  are  the  most 
frequent  source.  Syncope  and  death  may  occasionally  be  due  to 
cerebral  anemia,  from  afflux  of  blood  to  the  reexpanded  lung. 
Fatal  hemoptysis  has  followed  the  wounding  of  vascular  granu- 
lation tissue  in  the  lung  or  of  bloodvessels  lining  the  walls  or  travers- 
ing the  lumen  of  pulmonary  cavities.  Such  vessels  may  be  also  rup- 
tured during  expansion  of  the  lung.  Perforation  of  the  diaphragm 
has  been  followed  by  fatal  peritonitis  or  hemorrhage  from  the  spleen. 
Miliary  tuberculosis  may,  in  rare  instances,  arise  from  infected  thrombi 
set  free  from  pulmonary  vessels  by  the  evacuation  of  tuberculous  fluid 
(Frankel).  If  the  lung  is  adherent,  fatal  hemorrhage  from  pleural 
vessels  may  follow  forcible  aspiration.  Injury  of  an  atheromatous 
intercostal  artery  has  been  followed  by  fatal  bleeding  (Naunyn). 

Results  of  Thoracentesis. — Following  the  removal  of  fluid,  there  is 
usually  a  marked  improvement  in  the  breathing  and  cardiac  action. 
The  color  is  better  and  there  may  be  an  increase  in  the  amount  of 
urine.  The  heart  returns  to  its  normal  position  unless  prevented  by 
adhesions  or  marked  indurative  processes.  The  temperature  may  fall 
at  once,  but  gradual  defervescence  is  more  frequent.  The  duration 
and  intensity  of  the  pleuritis  appear  to  be  lessened.  Reexpansion 
of  the  lung  is  more  rapid,  absorption  of  the  remaining  fluid  takes 
place,  and  subsequent  deformity  with  contraction  of  the  side,  narrow- 
ing of  the  intercostal  spaces,  and  displacement  of  the  diaphragm  and 
heart  are  less  frequent.  It  is  a  mistake  to  regard  such  patients  as 
cured,  however,  for  too  often  the  subsequent  history  shows  that  the 
pleural  symptoms  have  been  relieved,  but  that  an  underlying 
tuberculous  process  continues  to  extend. 

In  some  cases  thoracentesis  is  actually  life-saving.  This  applies 
more  often  to  the  cases  in  which  early  diagnosis  of  the  tuberculous 
process  puts  both  patient  and  physician  in  possession  of  evidence 
without  which  only  half  measures  would  have  been  carried  out  in 
further  treatment.  It  also  applies  to  cases  with  alarming  pressure 
symptoms  in  which  evacuation  of  fluid  is  immediately  life-saving. 

After-treatment. — The  operation  of  thoracentesis  affects  the  general 
management  of  the  case  very  little.  If  the  patient  has  been  in  the 
reclining  position,  following  the  operation,  a  bed-rest  may  first  be 
given,  then  a  change  from  the  bed  to  a  chair,  and  the  patient  may  be 
up  and  about  by  the  end  of  a  week,  provided  no  contra-indications 
are  present.  This  interval  of  quiet  is  wise  even  if  all  goes  well,  to 
allow  time  for  readjustment  to  the  changed  intrathoracic  conditions 
and  repair  in  the  inflamed  pleura. 


518  DISEASES  OF  THE  PLEURA 

Avtoserotherapy.  Gilbert,1  Fede2  and  following  them  many  others 
have  treated  pleurisy  with  serofibrinous  effusion  by  the  subcutaneous 

injection  of  a  small  amount  of  aspirated  Huid.  The  usual  method 
has  been  to  inject  1  to  2  c.c.  and  if  necessary  repeat  the  injection 
even'  second-  day  until  as  many  as  four  to  six  injections  have  been 
given.  Improvement  in  the  patient's  genera]  condition  and  absorp- 
tion of  fluid  within  a  short  interval  have  been  observed  in  some 
cases  and  have  been  ascribed  to  entrance  into  the  circulation  of  anti- 
toxic and  bactericidal  substances  contained  in  the  effusion.  The 
results  have  not  in  general  been  sufficiently  striking  to  suggest  cura- 
tive action  by  the  serum.  Unfavorable  effects  have  not  been  observed. 
Wider  dissemination  of  tubercle  bacilli  is  a  possible  outcome  of  the 
procedure. 

ACUTE  PURULENT  PLEURITIS. 

Etiology. — Certain  differences  between  the  etiology  of  this  and 
other  forms  of  pleuritis  may  be  mentioned. 

Primary  Form. — The  proportion  of  cases  in  which  empyema  is 
apparently  primary  is  relatively  small  compared  with  fibrinous  and 
serofibrinous  pleuritis.  Of  252  cases  with  empyema  in  this  series, 
83  (32.9  per  cent.)  may  be  classed  in  this  group,  against  04  and  03  per 
cent.,  respectively,  for  the  fibrinous  and  serofibrinous  form.  Primary 
empyema  is  said  to  be  more  common  in  children,  but  expectoration 
is  often  absent  and  an  effusion  may  make  the  detection  of  a  pulmonary 
process  difficult  or  impossible. 

Secondary  Form. — As  in  other  varieties  of  pleuritis,  disease  of  the 
lung  occupies  frst  place  and  can  be  demonstrated  in  a  larger  pro- 
portion of  cases,  since  the  pulmonary  lesions  leading  to  suppuration, 
in  the  pleural  sac  are  more  easily  detected.  Of  252  cases,  158  (02.0 
per  cent.)  appeared  to  be  pulmonary  in  origin,  including  140  cases  of 
pneumonia  (130  lobar  pneumonia,  4  bronchopneumonia),  15  of  pul- 
monary tuberculosis  and  3  of  abscess  or  gangrene.  Gangrene  leads 
to  putrid  exudates.  The  disease  may  arise  by  extension  from  the 
abdomen,  the  pericardium,  or  the  other  pleura;  it  may  complicate 
the  infectious  diseases  (influenza,  typhoid  fever,  etc.)  or  suppurative 
lesions  in  any  part  of  the  body,  as  has  been  mentioned  for  the  other 
forms  of  pleuritis.  It  may  be  caused  by  trauma  and  may  follow  the 
serofibrinous  form. 

In  children  empyema  is,  in  general,  more  frequent  than  serofibrin- 
ous effusion.  There  is,  however,  considerable  variation  in  statistics 
on  this  point.  Of  109  cases  under  ten  at  St.  Bartholomew's  Hospital 
analyzed  by  Gee,  84  were  non-purulent,  85  purulent.  The  younger 
the  child,  the  more  likely  is  the  exudate  to  be  pus.  Thus,  of  Gee's  78 
cases  under  five,  53  were  purulent.  Of  110  cases  under  five  in 
Carpenter's  series,  77  were  empyema.  In  adults,  on  the  contrary, 
serofibrinous  effusions  are  much  more  common. 

1  Gaz.  d.  hop.,  1894,  p.  560.  2  Riforma  medica,  vol.  xxii,  No.  39. 


ACUTE  PURULENT  PLEURITIS  519 

1.  Pneumococcus. — This  appears  to  be  the  most  frequent  organism 
occurring  as  a  pure  infection.  Of  109  empyemas  investigated  by 
Netter,  it  was  present  in  53.6  per  cent,  of  28  cases  in  children,  while 
in  81  cases  of  adults  it  was  found  in  17.3  per  cent.  Of  137  cases 
in  my  series,  the  pneumococcus  was  found  in  54  (39.4  per  cent.). 
It  is  the  most  common  cause  of  metapneumonic  effusions,  but  may 
also  be  found  in  primary  empyema  and  shows  a  marked  tendency 
to  die  out.  It  may  be  found  in  smears  from  the  pus,  but  cultures 
from  the  same  fluid  are  not  infrequently  sterile.  To  this  is  probably 
due  the  relatively  favorable  course  of  pneumococccus  empyema.  It 
may  be  a  cause  of  suppuration  in  tuberculous  empyema,  in  which 
tubercle  bacilli  are  found  on  inoculation,  but  cultures  are  sterile  from 
the  disappearance  of  the  pneumococcus. 

2.  Streptococcus. — Netter  found  this  in  51  cases  (46.7  per  cent.). 
It  was  present   in  28  (20.4  per  cent.)  of  my  series.     Serofibrinous- 
effusions  containing  streptococci  are  likely  to  become  purulent. 

3.  Tubercle  Bacilli. — This  has  not  been  shown  to  be  as  frequent  a 
cause  of  purulent  as  of  serofibrinous  effusions.  Of  Netter's  109  cases, 
12  were  found  to  be  tuberculous.  The  finding  of  other  organisms  does 
not  exclude  the  tubercle  bacillus  nor  does  the  presence  of  the  tubercle 
bacillus  alone  exclude  other  organisms  such  as  the  pneumococcus, 
which  may  have  died  out. 

4.  Staphylococcus. — This  is  relatively  infrequent.  It  was  present 
in  only  one  of  Netter's  cases.  In  my  series  it  occurred  in  5  (3.6 
per  cent.). 

5.  Mixed  Infections,  etc. — Infection  with  more  than  one  organism 
was  found  in  22  (16  per  cent.).  The  pus  may  be  sterile,  as  in  25  cases 
(18.2  per  cent.),  and  infection  with  the  tubercle  bacillus  or  the  pneu- 
mococcus may  be  suspected.  Other  organisms  than  those  already 
mentioned  are  uncommon.  Influenza  bacilli,  typhoid  bacilli,  bacillus 
mucosus  capsulatus,  streptococcus  capsulatus,  diphtheria  bacillus, 
colon  bacillus,  actinomyces,  etc.,  have  been  found.  Mixed  infections 
are  usually  present  with  putrid  exudates.  The  investigations  of  Guil- 
lemot, Halle  and  Rist,1  Lorrain,2  Niosi3  and  others  suggest  that 
anaerobic  organisms  may  be  concerned  in  the  production  of  putrid 
pleural  exudates. 

Types  of  the  Disease. — The  purulent  pleurisies  have  been  separated 
into  different  groups  according  to  their  bacterial  etiology.  Mixed 
infections  with  one  or  more  organisms  are  common,  and  the  tubercle 
bacillus  may  coexist,  but  elude  detection.  Sterile  exudates  are  diffi- 
cult to  place;  they  are  usually  due  to  the  tubercle  bacillus,  rarely  to 
the  pneumococcus.  As  yet  no  distinctive  clinical  picture  can  be  form- 
ulated for  the  various  forms,  and  with  few  exceptions  the  clinical 
and  pathologic  similarity  of  the  different  infections  is  more  striking 
than  their  dissimilarity.    It  seems  best  to  consider  the  various  infec- 

1  Arch.  d.  med.  exp.,  1904.  2  Ibid.,  1902. 

3  Centralbl.  f.  Bakt.,  etc.,  i,  Abt.  Orig.,  1911,  Bd.  lviii,  H.  3,  p.  193. 


520  DISEASES  OF  THE  PLEURA 

tions  together  and  refer  to  such  differences  as  can   be  noted  under 

the  separate  headings. 

Pathology.  -The  pleura  is  the  site  of  a  fibrinous  or  fibrinopurulent 
layer.  It  is  grayish-white  or  yellowish  in  color,  and  may  be  greatly 
thickened.  The  inflammation  may  be  general  or  circumscribed.  The 
sacculation  of  fluid  is  not  infrequent.  Erosion,  ulceration,  or  even 
perforation  of  the  visceral  or  parietal  pleura  may  be  found.  These 
destructive  processes  may  be  single,  but  are  more  commonly  multiple 
and  limited  to  the  pulmonary  layer.  After  long-standing  empyema, 
allowed  to  run  its  course  untreated,  calcification  and  the  formation 
of  bony  plates  may  take  place  in  rare  instances. 

In  fatal  cases  other  organs  are  seldom  uninvolved.  The  lung  is  the 
most  frequent  site  of  changes,  from  which  the  pleural  disease  has 
usually  arisen  secondarily.  Lobar  pneumonia,  bronchopneumonia, 
abscess,  and  gangrene  may  be  the  source  of  the  process.  After  long- 
standing empyema,  chronic  interstitial  changes  may  occur  about  the 
lung  and  penetrate  the  pulmonary  tissue  along  the  interlobar  septa, 
the  so-called  pleurogenous  interstitial  pneumonia.  Suppurative  pul- 
monary lesions  and  bronchiectasis  are  likely  to  coexist.  It  is  often 
difficult  to  tell  whether  the  lung  is  primarily  or  secondarily  invaded. 
In  some  instances,  pleural  suppuration  extends  to  the  pericardium, 
peritoneum,  or  the  mediastinum,  from  which  the  opposite  pleura  may 
become  infected.  Endocarditis  is  not  uncommon.  The  spleen  may 
be  large  and  soft.  Thrombosis  of  intrathoracic  or  other  vessels  may 
be  present.  Cerebral  abscesses  may  occur.  Tuberculosis  of  the 
pleura,  lungs,  or  bronchial  glands  was  present  in  9  of  38  cases  at 
autopsy  in  my  series.  Tuberculous  lesions  in  more  remote  parts  of 
the  body  were  found  in  2.  Thus,  about  30  per  cent,  showed 
tuberculosis  in  some  part  of  the  body. 

Location. — Of  248  cases,  the  right  side  was  affected  in  122,  the  left 
in  121,  and  both  in  5.  Purulent  are  more  often  encapsulated  than 
serofibrinous  fluids.  Encapsulation  was  discovered  in  8  cases.  When 
empyema  complicates  pneumonia,  the  effusion  is  usually  at  the  bases 
irrespective  of  the  site  of  the  pneumonic  process. 

The  Effusion. — No  sharp  dividing  line  can  be  drawn  in  gross  appear- 
ance between  serofibrinous  and  purulent  fluids.  The  fluid  may  be 
merely  turbid,  with  a  few  fibrinous  flocculi  and  contain  an  excess 
of  poly  nuclear  cells  on  microscopic  examination.  It  must  be  remem- 
bered that  pus  may  sediment  within  as  well  as  outside  the  chest. 
At  operation  or  autopsy  tolerably  clear  serum  may  be  found  above 
with  a  layer  of  pus  at  the  bottom  of  the  pleural  sac.  The  effusion 
may  be  serofibrinous  at  first  and  become  purulent  later.  There  is 
often,  however,  an  excess  of  polynuclear  cells  in  such  fluids  from  the 
beginning.  The  fluids  may  be  yellowish,  with  varying  shades  of 
greenish,  reddish  or  even  frankly  red,  brownish  or  chocolate  colored 
from  the  presence  of  blood.  With  large  amounts  of  pus  they  are 
grayish,  greenish-yellow,  or  cream  colored.     They  may  be  without  odor, 


ACUTE  PURULENT  PLEURITIS  521 

sweetish,  or  fetid.  In  gangrene  of  the  lung  or  pleura  they  often  have 
a  horribly  offensive  odor.  The  specific  gravity  is  higher  than  in  sero- 
fibrinous fluids.  It  may  reach  1030  or  more.  The  amount  of  solids 
is  often  00  to  70,  but  may  reach  90  to  100  p.  m.  (Hummersten). 

Symptoms. — These  are  usually  the  same  as  in  the  serofibrinous 
form  and  only  certain  differences  need  be  mentioned.  They  are  not 
distinctive  of  empyema.  The  onset  is  likely  to  be  more  acute.  An 
insidious  onset  and  latent  course  are  less  common  than  in  the 
serofibrinous  form.  Toxic  symptoms  are  more  common  and  more 
severe.  In  general,  the  temperature  is  higher;  of  145  cases  only 
2  ran  an  afebrile  course.  From  101°  to  103°  is  an  average  pyrexia, 
but  the  temperature  reaches  104°,  105°,  or  even  higher  in  a  larger 
proportion  of  cases,  with  wider  variation  between  the  morning  and 
evening  elevations.  The  respiration  and  pulse  are  likely  to  be  more 
rapid.  Recurring  chilliness  or  chills,  a  more  rapid  loss  of  strength 
and  weight  and  increasing  pallor  may  be  mentioned.  Between  the 
various  infections  there  are  no  constant  differences.  Pneumococcus 
empyema  may  be  relatively  mild.  Streptococcus  infections  are  more 
severe,  and  putrid  exudates  are  accompanied  by  most  marked  dis- 
turbances. In  the  latter,  bad  taste  in  the  mouth,  foul  breath,  and 
foul  sputum  may  be  present.  Uncomplicated  tuberculous  effusions 
may  run  an  afebrile  and  long  course  without  marked  general  symp- 
toms. In  rare  instances  empyema  may  persist  without  symptoms 
for  months  or  years.  In  Faisans  and  Audistere's  case  the  disease 
may  have  lasted  for  forty  years.  At  autopsy  there  was  sterile  fluid 
contained  in  a  space,  the  walls  of  which  were  transformed  into  car- 
tilaginous and  osseous  tissue. 

Physical  Signs. — These  are  such  as  have  been  considered  under 
Serofibrinous  Effusion.  The  affected  side  may  be  more  prominent, 
with  wider  intercostal  spaces  which  may  actually  bulge.  Edema  of 
the  chest  wall  is  uncommon,  but  more  frequent  with  purulent  than 
with  serous  fluid.  The  subcutaneous  veins  may  be  dilated.  Whis- 
pered pectoriloquy  (Bacelli's  sign)  has  proved  an  uncertain  differ- 
entiation from  serofibrinous  pleuritis.  A  disproportion  between  the 
amount  of  fluid  and  the  severity  of  the  symptoms  may  be  suggestive. 
The  displacement  of  the  heart  and  the  liver  is  relatively  greater  with 
purulent  than  serofibrinous  fluid,  due  probably  to  the  greater  weight  of 
the  former.  In  children  the  breath  sounds  may  be  loud  and  bronchial 
over  a  purulent  effusion.  The  axillary  glands  are  occasionally  enlarged 
on  the  affected  side,  as  in  2  of  the  145  cases  in  my  series.  In  1, 
suppuration  was  present.  The  spleen  may  be  enlarged.  In  long-stand- 
ing cases,  especially  in  children,  clubbing  of  the  fingers  may  occur. 

Pulsating  Empyema. — This  condition  is  more  commonly  associated 
with  suppuration  in  or  about  the  pleural  sac.  Of  95  cases  analyzed 
by  Sailer1  there  was  pus  in  the  pleural  sac  in  71,  and  of  these  there 

1  Amer.  Jour.  Med.  Sci.,  1904,  cxxviii,  225. 


522  DISEASES  OF  THE  PLEURA 

was  tumor  (empyema  necessitatis)  in  3S.  In  13  there  was  intra- 
pleural or  extrapleural  abscess.  The  remaining  cases  were  non- 
purulent or  their  condition  was  not  definitely  known.  The  condition 
appears  to  be  more  common  in  males  and  in  early  life.  Pulsations 
may  be  diffuse"  or  localized,  single  or  multiple,  and  are  more  often 
seen  on  the  left  side.  They  are  most  common  in  the  parasternal  regions, 
but  may  occur  in  the  lower  lateral  and  posterior  parts  of  the  chest. 
Pulsation  is  probably  due  to  an  accumulation  under  pressure  of  fluid 
which  is  apposed  to  a  lung  made  inelastic  by  collapse  or  pathologic 
changes  in  or  about  it,  and  to  some  local  or  general  weakness  of  the 
thoracic  wall. 

The  Blood. — White  Cells. — In  28  cases  of  primary  empyema  the 
white  count  was  above  12,000  in  all  but  0,  i.  e.,  between  12,000  and 
10,000  in  3;  10,000  to  20,000  in  7;  20,000  to  24,000  in  4;  20,000  to 
35,000  in  3,  and  35,000  to  50,000  in  5.  The  0  cases  with  a  low  white 
count  recovered  after  operation.  No  conclusion  can  be  drawn  from 
the  white  count  in  this  small  number  of  cases  concerning  the  prog- 
nosis or  the  character  of  the  infecting  organism.  The  white  count 
may,  however,  be  of  great  value  in  distinguishing  uncomplicated 
tuberculous  serofibrinous  effusion  from  empyema,  only  3  of  33  cases 
with  the  former  showing  a  white  count  above  12,000. 

Complications. — These  are  much  the  same  as  for  serofibrinous  pleu- 
ritis. 

1.  Extension  to  Neighboring  Organs. — This  is  more  common  in  empy- 
ema, (a)  Perforation  of  the  Lung. — This  may  be  latent  and  indicated 
only  by  the  expectoration  of  mucopurulent  sputum.  Evacuation  of 
small  amounts  of  pleural  pus  by  this  means  is  frequent.  The  compli- 
cation is  frequently  overlooked  and  pneumothorax  only  rarely  occurs. 
In  other  cases  the  perforation  is  obvious.  In  this  form  pneumothorax 
is  more  common,  but  does  not  necessarily  occur.  There  is  a  sudden 
paroxysm  of  cough,  with  the  evacuation  of  a  large  amount  of  pus. 
If  perforation  occurs  while  the  patient  is  asleep  or  if  the  lung  is 
suddenly  flooded,  death  may  take  place  from  suffocation.  Single  or 
multiple  fistulous  tracts  may  connect  the  pleura  with  the  bronchi,  and 
pneumothorax  may  thus  arise.  Invasion  of  the  lung  usually  leads 
to  multiple  abscesses  connecting  with  the  bronchi.  In  some  instances 
the  affected  lung  may  present  a  honeycombed  appearance.  Single 
pulmonary  abscesses  are  less  common.  It  is  difficult  to  tell  in  indi- 
vidual cases  at  autopsy  whether  the  lung  has  been  primarily  or 
secondarily  involved.  Of  11  cases  with  pulmonary  suppuration  and 
empyema  at  autopsy,  abscesses  were  multiple  in  8,  single  in  3. 
Pulmonary  gangrene  may  occur,  but  is  less  common.  Chronic 
interstitial  pulmonary  changes  are  likely  to  follow  if  the  patient 
recovers.  Perforation  of  the  lung  was  absent  in  41  cases  of  pneu- 
mococcus  empyema;  present  in  2  of  19  streptococcus  cases.  It  is 
a  serious  event.  Of  145  cases,  obvious  perforation  occurred  in  5. 
One  patient  recovered.     A  second  had  persistent  cough,  with  abun- 


ACUTE  PURULENT  PLEURITIS  523 

dant  purulent  sputum  and  frequent  attacks  of  hemoptysis,  hut  was 
otherwise  well  six  years  after  the  operation.  The  3  remaining  patients 
died,  1  from  suffocation,  the  others  from  sepsis.  Evacuation  by  the 
lung  does  not  obviate  the  necessity  of  thoracotomy,  which  should 
be  done  to  spare  the  lung  from  further  damage.  Pulmonary  per- 
foration may  occur  at  any  time,  but  is  uncommon  before  the  third 
or  fourth  week. 

(b)  Perforation  of  the  Thoracic  Wall  (Empyema  Necessitatis). — 
This  is  less  common  than  pulmonary  perforation.  It  is  more  favor- 
able and  may  be  followed  by  complete  evacuation  and  recovery. 
The  abscess  may  point  in  any  part  of  the  chest,  but  more  often  in  the 
parasternal  region  or  in  the  fifth  interspace  outside  the  nipple  line, 
the  thinnest  regions  of  the  chest.  The  perforation  may  be  single 
or  multiple.  It  seldom  occurs  before  the  end  of  the  first  month,  but 
may  take  place  at  any  time  after  this  period.  The  abscess  usually 
forms  an  irreducible  fluctuating  tumor,  becoming  more  tense  with 
forced  expiration  or  cough.  It  is  dull  or  flat  on  percussion.  In  one 
case  a  reducible  resonant  tumor  was  present  in  the  left  second  inter- 
chondral  space,  shown  by  operation  to  be  due  to  pyopneumothorax. 
The  opening  into  the  thorax  may  be  at  some  distance  from  the  site 
of  the  tumor,  the  rupture  of  which  may  be  followed  by  discharge  of  a 
large  amount  of  fluid.  Forced  expiration  and  cough  may  hasten, 
inspiration  may  diminish  the  flow.  The  tumor  may  pulsate.  Evacu- 
ation by  spontaneous  perforation  is  usually  incomplete.  The  fistula 
is  likely  to  close  and  the  pleural  pus  to  reaccumulate,  with  subsequent 
perforation  in  the  same  or  other  places.  Cure  by  this  means  is  rare 
and  thoracotomy  is  indicated.  Caries  of  the  ribs  and  necrosis  of 
the  soft  parts  may  arise  from  the  perforation.  Erosion  of  an  inter- 
costal artery  may  lead  to  fatal  hemorrhage.  Perforation  is  more 
common  in  streptococcus,  tuberculous,  mixed,  or  putrid  infections. 
Actinomycosis  should  always  be  considered  in  the  presence  of  absces- 
ses of  the  chest  wall  arising  by  extension  from  within.  Simple  thoracic 
abscesses  may  be  unaccompanied  by  pulmonary  or  pleural  changes  and 
are  uninfluenced  by  changes  in  intrathoracic  pressure.  The  distinc- 
tion may,  however,  be  impossible  before  exploration  by  operation. 
Suppuration  in  the  tissue  between  costal  pleura  and  thoracic  wall 
(peripleuritis)  leading  to  external  perforation  may  simulate  encap- 
sulated empyema  necessitatis. 

(c)  Perforation  of  the  Diaphragm. — This  is  more  serious.  It  may 
lead  to  local  or  general  peritonitis.  As  in  perforation  of  the  lung,  it  is 
often  difficult  in  individual  cases  to  tell  whether  the  infection  has 
spread  from  the  pleura  to  peritoneum  or  in  the  opposite  direction. 
Obvious  gross  lesion  of  the  tissue  may  be  absent.  In  other  cases  the 
site  of  the  perforation  may  be  readily  found.  Peritonitis  was  present 
in  9  of  38  autopsies  on  cases  of  empyema  in  my  series.  It  was  general 
in  7,  localized  in  2.  Streptococci  were  present  in  7,  either  alone  or 
mixed  with  other  organisms.    In  one  case  an  encapsulated  diaphrag- 


524  DISEASES  OF   THE  PLEURA 

matic  empyema  pointed  in  the  right  hypochrondriuin;  recovery 
followed  operation.  In  a  case  of  pneumococcus  empyema  and  general 
pneumococcus  peritonitis  seen  with  C.  L.  Scudder,  recovery  followed 
repeated  abdominal  operations  and  eostateetomy.  An  abdominal 
abscess,  starting  from  the  pleura,  may  perforate  the  stomach,  the 
intestines,  or  the  kidney.  It  may  extend  along  the  spine  to  the  iliac 
fossa  and  simulate  psoas  or  lumbar  abscess. 

(r/)  The  esophagus  may  be  perforated,  as  in  the  cases  reported  by 
Vbelcker,  Thursfield,  and  Osier,  with  the  formation  of  pleuro- 
esophageal  fistula?. 

(e)  Infection  of  the  pericardium  is  probably  more  often  present 
than  statistics  show.  It  was  recognized  during  life  in  4  of  145  cases, 
but  was  present  at  autopsy  in  6  of  38.  Inflammation  may  also  extend 
to  the  mediastinum. 

2.  Metastatic  Lesions. — It  is  uncertain  in  individual  cases  whether 
suppurative  lesions  in  remote  parts  of  the  body  are  primary  or  second- 
ary. They  may  arise  by  extension  of  the  pleural  infection  to  the 
intrathoracic  veins  or  the  endocardium.  From  an  infected  thrombus 
thus  formed,  emboli  may  be  carried  to  the  brain,  kidney,  spleen,  or 
other  organs,  with  the  production  of  infarct  or  abscess.  Cerebral 
abscesses  are  among  the  most  dangerous  complications,  and  are  usually 
multiple,  as  in  3  of  38  autopsies  in  my  series.  Pulmonary  abscesses 
were  associated  in  2.  In  1  the  cerebral  abscesses  were  unaccom- 
panied by  suppurative  foci  elsewhere  than  in  the  pleura.  Septicemia 
is  common  in  empyema. 

3.  Amyloid  Degeneration  may  complicate  long-continued  suppuration. 
Causes  of  Death. — The  same  danger  of  sudden  death  and  similar 

causes  obtain  in  purulent  as  in  serofibrinous  effusion.  It  is  uncommon 
in  fatal  cases  not  to  find  suppurative  processes  in  neighboring  or 
other  parts  of  the  body.  Peritonitis  is  one  of  the  most  frequent  of 
coincident  infections,  and  Was  present  in  9  of  38  fatal  cases,  but  the 
complicated  character  of  fatal  cases  makes  it  difficult  to  judge  between 
principal  and  contributing  causes.  Pneumonia,  pulmonary  abscess 
and  gangrene,  pericarditis,  endocarditis,  thrombosis  of  intrathoracic 
veins  or  the  auricles,  with  or  without  infarction,  cerebral  abscesses, 
and  meningitis,  may  be  regarded  as  important  factors,  either  singly 
or  combined.  The  streptococcus  is  the  most  frequent  organism,  but 
pneumococci  are  often  present  and  other  organisms  may  be  found. 

Relapse. — Recurrence  of  empyema  in  the  same  place  after  com- 
plete recovery  does  not  occur,  because  of  the  almost  constant  oblitera- 
tion of  the  pleural  sac.  Incomplete  absorption  or  removal  may,  how- 
ever, be  followed  by  a  return  of  symptoms  and  an  increase  in  the 
amount  of  fluid.  Incomplete  evacuation,  insufficient  drainage,  encap- 
sulation, the  presence  of  undiscovered  pockets  of  pus  or  the  develop- 
ment of  empyema  elsewhere  may  be  responsible  for  a  second  accumu- 
lation of  fluid.     Pitt1  reported  the  unusual  postmortem  finding  of  a 

1  British  Med.  Jour.,  1908,  ii,  1075. 


ACUTE  PURULENT  PLEURITIS  525 

smooth  pleural  surface  without  adhesions  in  a  child  who  had  empyema 
one  year  before. 

Sequelae. — It  is  rare,  on  physical  examination  of  patients  who  have 
recovered  from  empyema,  not  to  find  signs  of  the  previous  disease. 
There  is  diminished  expansion  of  the  affected  side,  which  often  looks 
smaller,  and  measurement  shows  that  it  is  contracted.  The  inter- 
spaces are  relatively  narrow.  Toward  the  base  is  slight  relative  dul- 
ness,  its  upper  limit  often  being  highest  behind  and  extending  in  a 
nearly  horizontal  line  toward  the  axilla,  where  it  gradually  descends 
to  the  inferior  pulmonary  margin  in  the  anterolateral  thoracic  region. 
The  extent  of  dulness  is  variable  and  may  involve  half  the  chest. 
The  tactile  fremitus  may  be  diminished  over  the  dull  area.  The 
breathing,  voice  sounds,  and  whisper  may  be  diminished,  but  are 
often  unchanged.  In  cases  which  have  run  a  long  course  before 
evacuation  takes  place,  with  abundant  connective-tissue  formation 
about  the  lung  or  within  its  substance,  the  lung  may  be  partially  or 
wholly  incapable  of  reexpansion.  A  space  is  left  which  is  filled  by 
fibrous  tissue,  by  the  collapse  of  the  chest  wall,  dislocation  of  the 
mediastinum  and  heart  toward  the  affected  side,  displacement  upward 
of  the  diaphragm  and  partial  expansion  of  the  lung,  depending  on 
the  changes  which  have  taken  place  in  and  about  it.  In  rare  cases, 
with  dulness,  there  may  be  signs  suggestive  of  slight  degrees  of  pul- 
monary solidification.  These  may  be  due  to  interstitial  changes  in 
the  lung,  or,  if  marked  retraction  has  taken  place,  to  proximity  of  the 
larger  bronchi  to  the  chest  wall.  In  the  young,  with  less  resistant 
thoracic  walls,  marked  deformity  with  retraction  of  the  side,  droop- 
ing of  the  shoulder  and  lateral  deviation  of  the  spine  may  result. 

Pain  of  variable  and  usually  slight  intensity  may  persist  in  the 
affected  side.  Of  26  patients  investigated  on  this  point,  8  still  had 
pain  for  periods  of  one  to  seven  years  after  discharge. 

Diagnosis. — The  diseases  with  which  pleural  effusion  may  be 
confused,  the  differentiation  of  pleural  fluids  of  different  character, 
the  method  of  employing  exploratory  puncture  and  the  examination 
of  pleural  fluids  have  already  been  discussed  under  Serofibrinous 
Pleuritis. 

Certain  additional  features  in  the  diagnosis  of  empyema  may  be 
emphasized  with  special  reference  to  exploratory  puncture,  exploratory 
incision,  and  the  examination  of  purulent  fluid. 

Exploratory  Puncture. — This  is  indicated  if  pus  is  suspected.  By 
hesitation  and  delay,  the  disease  may  be  converted  into  a  chronic  and 
incurable  affection.  In  acute  cases,  with  typical  signs  of  fluid,  it  is 
practically  devoid  of  danger,  and,  if  present,  pus  can  usually  be  demon- 
strated by  this  means.  In  some  cases,  however,  it  is  missed  by  the 
trocar  or  is  too  viscid  to  flow.  A  negative  puncture  does  not  exclude 
pus. 

Cases  in  which  Exploratory  Puncture  is  Dangerous. — In  cases  of 
empyema  of  long  standing,  in  which  there  is  contraction  of  the  side, 


526  DISEASES  OF  THE  PLEURA 

elevation  of  the  diaphragm,  and  secondary,  suppurative  lesions  in 
the  lung,  or  in  cases  in  which  empyema  complicates  pulmonary  abscess, 
gangrene*  bronchiectasis,  and  interstitial  pneumonia,  the  conditions 
are  less  favorable  for  exploratory  puncture.  The  pleural  pus  is  often 
small  in  amount,  and  may  be  encapsulated  between  lung  and  diaphragm 
or  in  other  parts  of  the  chest.  The  diagnosis  of  pleural  involvement 
in  the  cases  under  consideration  can  usually  be  made.  The  history 
may  afford  important  evidence.  Lobar  pneumonia  and  infection  of 
the  thorax  from  without  never  spare  the  pleura.  There  may  be  a 
history  of  pain  characteristic  of  pleural  invasion  or  symptoms  con- 
sistent with  the  rupture  of  empyema  into  the  lung.  The  physical 
signs  may  be  atypical,  but  if  the  pus  reaches  the  chest  wall,  localized 
tenderness,  dulness  or  flatness  on  the  affected  side  and  the  opposite 
paravertebral  region,  diminished  or  absent  breathing  and  voice  sounds, 
with  tegophony,  and  the  absence  of  tactile  fremitus,  whispered 
pectoriloquy  and  the  diaphragm  shadow  may  disclose  the  presence 
of  an  effusion.  It  is  well  to  confirm  the  results  of  physical  examina- 
tion by  radioscopy.  Exploratory  puncture  is  not  without  danger  in 
cases  thus  complicated.  Bloodvessels  lining  the  walls  or  traversing 
the  lumen  of  pulmonary  cavities  or  fresh  granulation  tissue,  if  injured 
by  the  trocar,  have  been  the  source  of  fatal  hemorrhage.  Perfora- 
tion of  the  elevated  diaphragm  has  caused  fatal  peritonitis.  In  the 
presence  of  such  complications,  with  typical  signs  of  fluid  and  dis- 
placement of  the  heart,  exploratory  puncture  may  be  made,  but 
with  care  not  to  introduce  the  instrument  too  far  or  through  the 
diaphragm,  the  position  of  which  should  be  determined  by  .r-ray 
examination.  In  similarly  complicated  cases,  in  which  from  the  his- 
tory, the  physical  signs,  and  the  .r-ray  examination  there  is  good 
reason  to  suspect  pus,  the  demonstration  of  which  with  the  trocar 
has  failed  or  cannot  be  safely  undertaken,  it  is  better  to  resort  to 
exploratory  incision. 

Exploratory  Incision. — This  is  indicated,  as  already  mentioned, 
when  there  is  good  reason  to  suspect  pus  wrhich  cannot  be  demon- 
strated by  exploratory  puncture  or  in  complicated  cases  in  which 
it  is  a  less  dangerous  procedure.  It  should  .be  entrusted  only  to  an 
experienced  surgeon.  The  technic  of  operation  cannot  be  considered 
here.  The  chief  danger  is  artificial  pneumothorax,  which  may  arise 
if  the  lung  is  free.  Incision  and  costatectomy,  with  care  not  to  wound 
the  pleura,  will  disclose  the  condition  of  the  underlying  tissue. 

Examination  of  Pleural  Pus. — Fluids  on  the  border  line  between 
the  serofibrinous  and  purulent  variety  may  be  examined  as  already 
indicated  in  the  preceding  section.  Cultures  should  always  be  made. 
With  frank  pus,  tubercle  bacilli  may  be  demonstrated  by  the  follow- 
ing means:  A  few  cubic  centimeters  are  transferred  to  a  flask  and 
diluted  with  10  volumes  of  water.  A  few  drops  of  strong  alkali 
(KOH  or  XaOH)  are  added  and  the  solution  is  gently  heated.  After 
the  cellular  elements  are  dissolved,  the  solution  may  be  centrifugal- 


ACUTE  PURULENT  PLEURITIS  527 

ized  and  the  precipitate  investigated  for  tubercle  bacilli.  Animals 
cannot  be  inoculated  with  large  amounts  of  pus  or  intraperitoneal  I y, 
without  a  too  rapidly  fatal  termination  for  the  demonstration  of 
tuberculosis.  It  is  best,  therefore,  to  inject  only  1  to  2  c.c.  of  pus 
under  the  skin. 

Prognosis. — Absorption  of  empyema  rarely,  if  ever,  occurs.  Spon- 
taneous disappearance  of  pus  has  been  noted  in  isolated  cases  by 
Fiirbringer,  Gerhardt,  Frankel,  Schede,  and  others.  It  may  be  due 
to  latent  perforation  of  the  bronchi.  Recovery  may  follow  obvious 
perforation  of  the  lung,  but  usually  with  most  distressing  and  danger- 
ous complications.  After  perforation  of  the  chest  wall  recovery  may 
follow.  Most  cases,  if  untreated,  end  in  death.  Of  252  cases  in  my 
series  56  (22.2  per  cent.)  died  in  hospital. 

Treatment. — In  general,  pleural  pus  should  be  evacuated  as  soon  as 
the  diagnosis  is  made.  Constant,  free  drainage  is  essential  for  prompt 
and  permanent  cure. 

1.  Thoracotomy  with  Costatectomy. — This  is  the  operation  of  choice. 
The  incision  is  best  made  in  a  dependent  part  of  the  pleural  cavity, 
with  resection  of  the  seventh  or  eighth  rib  in  the  posterior  axillary 
line.  Pus  should  be  evacuated  slowly.  Irrigation  of  the  cavity  is 
seldom  necessary  and  may  be  dangerous.  With  empyema  necessitatis, 
enlargement  of  the  perforation  in  the  chest  wall  may  suffice  if  this 
is  in  a  favorable  position  for  drainage.  Otherwise,  a  second  opening 
in  a  more  suitable  position  should  be  made.  If  the  pus  is  encapsu- 
lated, the  incision  must  be  made  where  drainage  will  be  most  effective. 
Thoracotomy  alone  often  affords  insufficient  drainage  and  costatec- 
tomy is  often  necessary  later. 

2.  Other  Methods. — These  are  less  efficient  since  drainage  is  often 
neither  constant  nor  free,  but  they  may  be  used  in  selected  cases,  as 
a  preliminary  to  the  radical  operation  or  as  palliative  procedures. 
"  (a)  Thoracentesis. — This  may  be  considered  for  effusions  on  the 
border  line  between  the  serofibrinous  and  purulent  forms.  It  is  indi- 
cated for  the  evacuation  of  an  exudate  of  large  size,  with  or  without 
pressure  symptoms,  as  a  life-saving  measure  or  a  preliminary  to  opera- 
tion, thus  avoiding  the  danger  of  more  rapid  evacuation,  and  as 
a  palliative  procedure  in  empyema  complicating  advanced  pulmonary 
tuberculosis.  Although  repeated  puncture  has  been  advised  for 
pneumococcus  empyema,  especially  in  children,  it  is  uncertain,  likely 
to  be  followed  by  re-accumulation,  and  leads  to  complications  and 
greater  deformity  of  the  chest.  It  frequently  delays  operation,  which 
is  often  necessary  later,  and  subjects  the  patient  to  an  unjustifiable  risk. 

(b)  Siphon  Drainage  ( Bulau) .  —  By  this  method1  drainage  is 
afforded,  but  evacuation  is  often  neither  constant  nor  free.     Slow 

1  A  trocar  6  to  7  mm.  in  diameter  and  armed  with  a  stop-cock  is  inserted  through 
the  seventh  or  eighth  axillary  space.  Through  this  a  rubber  catheter  is  passed  and 
the  trocar  withdrawn.  One  end  of  a  short  piece  of  glass  tubing  is  inserted  into  the 
free  end  of  the  catheter,  the  other  into  a  rubber  tube,  leading  to  a  receptacle,  attached 
to  the  bed  or  placed  on  the  floor. 


528  DISEASES  OF   THE   PLEURA 

evacuation,  avoidance  of  narcosis,  and  a  large  operation  wound, 
no  danger  of  pneumothorax,  and  hotter  expansion  of  the  retracted 
lung  are  advantages  claimed  for  the  method.  The  apparatus  requires 
constant  attention,  pus  is  less  likely  to  be  completely  evacuated, 
and  masses  of  fibrin  may  readily  obstruct  the  tube.  Fluid  may  escape 
or  air  enter  about  the  tube.  It  is,  therefore,  more  suitable  for  hos- 
pital patients  or  where  constant  attention  is  possible.  It  may  be 
tried  at  the  extremes  of  age,  in  weak  patients  unable  to  stand  the 
radical  operation,  in  relatively  benign  pneumococcus  empyema, 
without  much  fibrin,  and  in  double  empyema,  in  which  collapse  of 
the  lung  from  pneumothorax  is  to  be  avoided. 

Tuberculous  Empyema. — In  this  form  the  indications  are  less  clear 
and  considerable  difference  of  opinion  exists  concerning  the  appro- 
priate treatment.  In  an  advanced  stage  of  the  disease  a  radical 
operation  can  hardly  be  considered,  and  such  palliative  measures 
as  repeated  puncture  or  siphon  drainage  may  he  tried.  The  decision 
is  more  difficult  when  empyema  complicates  early  pulmonary  tuber- 
culosis. If  the  exudate  is  sterile  or  contains  tubercle  bacilli  alone, 
aspiration  may  be  tried.  If  the  fluid  reaccumulates,  aspiration  may 
be  repeated.  Thoracotomy  and  costatectomy  are  likely  to  be  followed 
by  the  formation  of  a  persistent  sinus.  If  the  fluid  contains  pyogenic 
cocci,  thoracotomy  combined  with  costatectomy  is  the  operation  of 
choice.  Of  31  cases  of  tuberculous  empyema  operated  by  Ktister,  9 
recovered,  6  were  not  cured,  and  16  died.  In  Schede's  collective  investi- 
gation of  45  cases,  10  were  cured  and  35  died,  a  mortality  of  77  per 
cent.  In  general,  tuberculous  empyema  is  the  most  unfavorable 
form.  Of  12  cases,  with  sterile  exudates,  in  my  series,  only  1  of 
whom  showed  tubercle  bacilli  in  the  sputum,  3  died  in  hospital.  Of 
the  remaining  9  patients,  6  have  been  traced.  All  have  died  except  1, 
who  had  a  discharging  sinus,  seven  years  after  operation,  but  was 
otherwise  well.  Sterile  exudates  are  usually,  but  not  necessarily, 
tuberculous. 

After-treatment. — Expansion  of  the  lung  may  be  favored  by  various 
devices,  permitting  the  outflow  of  pus  and  air  through  the  drainage 
tubes  during  expiration,  but  preventing  the  reentry  of  air  during 
inspiration.  A  thin  layer  of  impervious  material  (mackintosh,  pro- 
tective silk)  may  be  applied  over  the  opening  of  the  tubes.  The 
dressing  itself,  when  soaked  with  secretion,  may  suffice.  A  vacuum 
apparatus  may  be  used  as  in  Perthes'  method.  After  closure  of  the 
sinus,  respiratory  exercises  are  valuable.  Throughout  the  illness, 
every  means  should  be  taken  to  build  up  the  general  health. 

Vaccination. — The  subcutaneous  inoculation  of  vaccines,  according 
to  Wright's  method,  may  be  considered  in  the  absence  of  auto- 
inoculation  and  for  the  treatment  of  a  persistent  sinus.  Their  value 
must  be  left  for  the  future  to  decide.  According  to  present  indica- 
tions and  my  own  experience,  the  control  of  the  dosage  by  the 
opsonic  index  is  unreliable. 


ACUTE  PURULENT   PLEURITIS  529 

Results  of  Operation. — The  mortality  of  the  operation  itself  is  very 
low.  In  patients  already  near  the  end,  it  may  hasten  the  fatal  ter- 
mination, but  even  in  the  most  desperate  cases  evacuation  by  some 
means  is  justifiable. 

1.  Immediate  Results. — The  success  or  failure  of  operation  is  largely 
dependent  on  the  period  at  which  the  disease  is  discovered,  the  char- 
acter of  the  underlying  process,  and  the  infecting  organisms.  Too 
much  reliance,  however,  cannot  be  placed  on  these  factors  in  individ- 
ual cases.  In  general,  the  results  are  much  more  favorable  when  the 
empyema  is  detected  early.  Concerning  the  character  of  the  under- 
lying disease,  tuberculous  cases  are  most  unfavorable.  Of  45  opera- 
tions on  tuberculous  empyema  in  Schede's  collected  cases,  there  was 
a  mortality  of  77  per  cent,  and  an  average  duration  of  136  days  from 
operation  to  recovery  in  favorable  cases.  Judging  from  Schede's 
cases,  secondary  and  metastatic  empyema  stands  next  in  the  number 
of  fatalities,  with  a  mortality  of  32  per  cent,  in  50  cases.  Of  288 
metapneumonic  empyemas,  the  mortality  was  13  per  cent,  with  an 
average  of  83  days  for  recovery,  while  idiopathic  empyema  was 
most  favorable  with  a  mortality  of  7.9  per  cent,  among  101  cases 
and  66  days  for  recovery.  In  regard  to  the  relation  between  the  imme- 
diate results  and  the  infecting  organisms,  the  duration  of  the  process, 
the  character  of  the  underlying  disease,  the  presence  of  complica- 
tions and  various  other  factors  must  be  considered.  Large  series 
of  cases  are  lacking.  To  judge  from  my  small  series,  excluding 
obviously  tuberculous  cases,  the  mixed  infections  seem  to  be  most 
favorable.  Of  27  cases  in  this  group  (mostly  pneumococcus  and 
streptococcus,   and  including  8    primary,   18    metapneumonic,    and 

1  with  abscess  of  the  lung),  5  (18.5  per  cent.)  died  in  hospital. 
Of  the  fatal  cases,  1  was  primary,  the  others  metapneumonic. 
The  pneumococcus  cases  appear  to  stand  next  in  the  number  of 
fatalities,  for  of  35  cases  (including  6  primary,  26  metapneumonic, 

2  following  trauma,  and  1  complicating  measles),  only  4  (11.4  per 
cent.)  died  in  hospital.  Of  the  fatal  cases,  1  was  primary,  3  were 
metapneumonic.  The  mortality  of  the  streptococcus  cases  was  even 
lower.  Of  17  pure  streptococcus  infections  (8  primary,  9  metapneu- 
monic), only  1  (5.8  per  cent.)  metapneumonic  case  died  in  hospital. 
Streptococcus  cases  are  usually  considered  especially  unfavorable. 
Judging  the  severity-  of  the  different  infections  by  the  average  stay 
in  hospital  from  operation  to  discharge,1  there  is  no  striking  differ- 
ence between  the  different  groups.  For  the  mixed  infections  the 
average  duration  was  forty-five  days,  for  the  pneumococcus  cases 
thirty-five  days,  and  for  the  streptococcus  thirty-eight  days. 

2.  Remote  Results. — The  chief  interest  lies  in  the  possibility  of 
tuberculosis.  Of  13  cases  of  primary  empyema  4  have  died — 2  of 
"empyema"  at  intervals  of  six  and   eleven  months  after  discharge, 

1  Fatal  cases  are  not  included.     The  duration  is  short,  for  patients  with  sinus  are 
discharged  to  a  convalescent  home. 
34 


530  DISEASES  OF   THE  PLEURA 

1  of  an  unknown  cause  after  one  year  and  the  last  from  intus- 
susception. The  remaining  9  patients  are  well  at  an  average 
interval  of  four  years  after  discharge.  Of  2(i  patients  with  meta- 
pneumonic empyema,  7  have  died — 2  of  "empyema"  after  one  and 
four  years,  1  of  "pneumonia,"  1  of  "tuberculosis,"  and  the  remain- 
ing patients  from  causes  unconnected  with  this  disease.  Of  the  re- 
maining 19  patients,  1  is  known  to  have  pulmonary  tuberculosis,  2 
others  have  had  hemoptysis,  and  a  third  has  a  persistent  pleural 
sinus,  seven  years  after  discharge.  The  patients  who  are  still  alive 
have  been  followed  for  an  average  period  of  about  five  years.. 


CHAPTER  XXX. 
SPECIAL  FORMS  OF  PLEURITIS. 

(1)  Diaphragmatic  Pleurisy. — Pleuritis  may  be  limited  to  the 
diaphragmatic  region.  It  may  be  partial  or  general,  fibrinous,  sero- 
fibrinous, or  purulent.  Large  collections  of  fluid  are  rare.  Owing 
to  its  inaccessible  site,  physical  signs  are  often  lacking  and  the  diag- 
nosis may  rest  on  symptoms  alone.  The  pain  may  present  features 
already  described  under  Fibrinous  Pleuritis,  but  is  more  likely  to  be 
referred  to  the  lower  thoracic  or  abdominal  region.  This  may  be 
due  to  implication  of  the  lower  intercostal  nerves  which  supply  the 
skin  and  muscles  of  the  abdominal  wall,  as  well  as  the  parietal  and 
diaphragmatic  pleura.  In  my  series,  abdominal  pain  was  noted 
in  5  of  82  cases  with  primary  fibrinous,  in  5  of  374  cases  with 
primary  serofibrinous,  and  in  2  of  33  cases  of  primary  purulent  pleu- 
ritis. It  may  be  associated  with  muscular  spasm  and  tenderness, 
and  the  picture  may  simulate  an  acute  abdominal  affection  for 
which  laparotomy  has  been  performed.  Herrick1  has  emphasized 
its  importance  as  a  symptom  of  pleural  and  pulmonary  disease. 
W.  B.  James  suggests  that  aggravation  of  pain,  following  fixation 
of  the  thorax  with  straps,  and  its  relief  when  the  abdomen  is  similarly 
immobilized,  may  indicate  the  diaphragmatic  site  of  pleurisy.  There 
may  be  tenderness  over  the  phrenic  nerve  in  the  neck  or  at  the  inter- 
section of  a  vertical  line  parallel  to  the  outer  margin  of  the  sternum 
and  a  horizontal  line  continuous  with  the  termination  of  the  tenth  rib 
(De  Mussy's  Bouton  Diaphragmatique) .  The  breathing  may  be 
partially  or  wholly  thoracic  in  type  and  the  diaphragm  phenomenon 
absent  on  one  or  both  sides  of  the  chest.  Dyspnea  may  be  marked 
and  attacks  simulating  angina  may  be  observed  (Andral).  Obstinate 
singultus  may  occur.  In  a  recent  patient  with  diaphragmatic  pleu- 
risy, it  was  the  principal  trouble  for  which  relief  was  sought.  The 
phrenic  and  pharyngeal  branches  of  the  vagus  nerve  are  implicated 
and  probably  through  irritation  of  the  former  in  the  diaphragm.  The 
swallowing  of  food  may  cause  pain. 

(2)  Encysted  Empyema, — Encapsulation  of  uncomplicated  transu- 
dates does  not  occur.  It  is  rare  with  serofibrinous  fluid,  but  more 
common  with  pus.  In  occasional  instances  fluid  may  be  serous  in 
one  and  purulent  in  another  pocket.  Sacculation  was  discovered  in 
only  1  of  1085  cases  of  serofibrinous  effusion,  but  in  8  (3.2  per 
cent.)  of  248  empyemas  in  this  series.  It  is,  however,  probably 
much  more  common  that  these  figures  show,  for  in  38  autopsies  on 

1  Illinois  Med.  Jour.,  1903-04,  N.  S.,  v,  603. 


532  DISEASES  OF  THE   PLEURA 

patients  with  empyema  it  was  noted  in  12  (31.5  per  cent.).  Sac- 
culation is  more  likely  to  occur  in  small  or  medium  effusions  and  in 
those  in  which  the  fluid  is  at  a  standstill.  Encapsulation  may  occur 
between  (1)  diaphragm  and  lung,  (2)  the  lung  and  chest  wall,  and  (3) 
the  lobes  of  the  lung. 

(a)  Encapsulation  of  Pus  between  Diaphragm  and  Lung  is  more  com- 
mon than  in  other  situations.  In  most  instances  the  empyema  is  at 
first  free,  but  is  later  walled  off  by  adhesion  of  inflamed  and  apposed 
pleural  surfaces  in  the  posterior  and  inferior  thoracic  region.  This  was 
noted  in  five  autopsies  in  the  present  series.  Sacculation  of  fluid 
above  the  diaphragm  without  apposition  to  the  thoracic  wall  may 
occur.  The  effusion  may  be  bounded  by  lung  and  diaphragm,  or 
by  lung,  diaphragm,  and  the  mediastinum.  Perforation  of  lung 
or  diaphragm  may  be  the  first  objective  sign  of  the  disease.  The 
symptoms  may  suggest  diaphragmatic  pleurisy.  The  heart  and  the 
organs  below  the  diaphragm  may  be  dislocated,  expansion  of  the 
affected  side  may  be  deficient,  and  on  systematic  examination  of  the 
chest  an  area  of  impaired  resonance  several  inches  above  the  base 
of  the  lung  may  be  discovered.  In  this  region  diminished  breathing, 
voice  sounds,  and  tactile  fremitus  may  be  suggestive.  Pleuritic 
friction  may  occur.  If,  as  is  often  the  case,  more  extensive  pleuritis 
has  preceded  the  sacculation,  the  physical  signs  may  be  difficult  of 
interpretation. 

(b)  Sacculation  between  Lung  and  Chest  Wall. — This  is  not  uncom- 
mon and  is  likely  to  occur  in  cases  in  which  a  previous  pleuritis  has 
obliterated  the  diaphragmatic  portion  of  the  pleural  sac.  It  is  occa- 
sionally observed  in  empyema  in  which,  following  operation,  the 
sinus  has  been  allowed  to  close  too  quickly.  Such  encapsulation  is 
more  common  over  the  base,  but  may  be  observed  over  other  parts 
of  the  lung. 

(c)  Interlobar  Empyema.  —  Inflammation  of  the  interlobar  pleura 
occurs  as  part  of  a  general  pleuritis.  An  effusion  of  fluid  may  be 
limited  externally  by  the  thoracic  wall,  internally  by  the  lobes  of  the 
lung  between  which  it  lies.  In  rare  instances  the  effusion  may  not 
extend  to  the  chest  wall,  and  is  bounded  on  all  sides  by  the  lung. 
The  symptoms  are  not  distinctive  and  the  diagnosis  is  difficult. 
Examination  may  be  negative  and  perforation  of  the  lung  may  be 
the  first  indication.  Rupture  may  take  place  as  early  as  the  four- 
teenth (Potain)  or  the  nineteenth  (D.  Gerhard t)  day.  Dislocation 
of  the  heart  may  occur.  In  the  affected  region  there  may  be  dulness, 
diminished  or  absent  breathing,  voice  sounds,  and  tactile  fremitus. 
The  localization  of  the  process  in  the  region  of  the  interlobar  septa 
and  the  absence  of  signs  above  and  below  this  region  are  most  likely 
to  suggest  the  diagnosis.  Examination  by  means  of  the  a>rays  may 
be  of  great  assistance.     Sacchonaghi1  has  reviewed  the  literature. 

1  Gesamt.  geb.  d.  prakt.  Med.,  1910,  x,  151. 


ANTINOMYCOSIS  OF  THE  PLEURA  533 

Diagnosis. — Laennec  regarded  segophony  as  an  important  sign. 
Localized  tenderness  may  be  elicited  by  firm  and  deep  pressure  in 
the  interspaces.  Sacculated  and  especially  interlobar  empyema  is 
likely  to  be  confused  with  pulmonary  abscess.  The  gross  character 
of  the  sputum  may  be  suggestive.  The  sudden  expectoration  of  a 
large  amount  of  homogeneous  pus,  little  mixed  with  mucus,  may 
suggest  empyema.  The  discovery  in  the  expectoration  of  elastic 
tissue  with  an  alveolar  arrangement  is  diagnostic  of  pulmonary 
abscess,  but  does  not  exclude  a  complicating  empyema.  Tumors  of 
the  lung  must  also  be  considered.  Exploratory  puncture  is  usually 
recommended  for  the  diagnosis,  but  its  danger  has  already  been  noted 
(p.  525),  and  exploratory  incision  may  be  safer. 

Treatment. — Perforation  of  the  lung  has  been  followed  by  spon- 
taneous recovery.  If  perforation  has  already  occurred  when  the 
patient  comes  under  observation,  the  decision  between  an  expectant 
policy  and  operation  must  be  made  on  the  exigencies  of  the  individual 
case.     If  the  empyema  can  be  reached,  its  evacuation  is  indicated. 

(3)  Actinomycosis  and  Streptothricosis  of  the  Pleura. — Two  kinds 
of  parasites  must  be  recognized,  i.  e.,  Actinomyces  bovis  and  Strep- 
tothrix.  Although  the  two  parasites  present  well-marked  biologic 
differences,  the  clinical  and  pathologic  picture  in  infection  is,  in 
general,  quite  similar. 

Actinomycosis. — In  a  large  proportion  of  the  cases  this  arises  by 
extension  from  the  lung.  Pleural  invasion  may  also  occur  from  the 
esophagus;  by  extension  downward  from  the  neck  to  the  mediasti- 
num and  thence  into  the  pleura,  or  from  abdominal  lesions  which 
perforate  the  diaphragm.  Metastasis  is  a  possible  mode  of  origin. 
The  pleura  overlying  the  involved  tissue  is  the  site  of  a  fibrinous 
exudate.  If  adhesion  of  the  visceral  and  parietal  layers  does  not 
take  place,  a  serofibrinous  effusion  or,  more  commonly,  an  empyema 
may  result.  The  manifestations  on  the  part  of  the  pleura  may  mask 
the  primary  focus  of  the  disease.  Perforation  of  the  chest  wall  is  a 
characteristic  feature.  If,  as  often  happens,  pleural  adhesion  pre- 
cedes the  perforation,  extension  takes  place  through  an  obliterated 
pleural  sac  and  the  pleural  changes  are  merely  an  incident  in  a  more 
obvious  disease  of  other  organs.  The  thoracic  wall  may  be  involved 
without  extensive  changes  in  the  pleura,  or  suppuration  may  similarly 
perforate  the  diaphragm  by  extension  downward  from  the  lung  or 
upward  from  the  abdomen,  without  invasion  of  the  general  pleural 
space.  It  is  the  site  of  single  or  multiple  indurated  and  suppurating 
areas,  connecting  by  means  of  sinuses  with  the  pleura  or  the  pleura 
and  lung.  Perforation  may  take  place  at  any  part  of  the  thorax,  but 
is  more  common  in  the  lower  thoracic  region.  Erosion  of  the  ribs 
may  occur.  Amyloid  degeneration  may  follow  long-continued  sup- 
puration. 

There  is  no  distinctive  clinical  picture.  Actinomycosis  should  be 
suspected  in  empyema,  especially  when  associated  with  chronic  pul- 


534  DISEASES  OF   THE  PLEURA 

monary  suppuration,  interstitial  pneumonia,  abscess,  gangrene,  or 
empyema  necessitatis.  The  diagnosis  can  be  made  only  by  finding 
granules  with  branching,  Gram-staining  filaments  and  radially  dis- 
posed club-shaped,  eosin-staining  peripheral  bodies.  The  prognosis 
is  very  unfavorable.  A  few  arrested  or  apparently  cured  eases  have 
been  reported.  The  treatment  is  surgical,  combined  with  the  internal 
administration  of  large  doses  of  iodid  of  potassium. 

Streptothricosis. — This  appears  to  be  much  less  common.  Infection 
of  the  pleura  takes  place  by  extension  from  the  lung.  The  changes 
are  similar  to  those  in  actinomycosis,  and  may  closely  resemble 
tuberculosis.  The  diagnosis  is  made  by  finding  thread-like,  branch- 
ing organisms,  which,  in  most  cases,  resist  decolorization  with  weak 
acids  and  alcohol,  but  are  less  "acid-fast"  than  the  tubercle  bacillus, 
do  not  form  granules  or  masses  of  closely  packed  interlacing  fila- 
ments with  the  characteristic  "clubs"  at  the  periphery  and  are 
much  more  readily  cultivated  than  either  tubercle  bacilli  or  actino- 
myces.  In  Birt  and  Leishman's  case1  an  "acid-fast"  streptothrix  was 
recovered  from  the  lung  and  the  pleural  pus.  Lebram2  reports  a  case 
which  appears  to  belong  in  this  group.  There  wTere  multiple  pulmo- 
nary abscesses  and  bilateral  pleuritis.  The  left  pleura  contained  gray, 
pearl-gray,  or  white  nodules,  resembling  miliary  tubercles,  in  which, 
as  well  as  in  the  lungs,  branching  threads  were  found,  but  no  tubercle 
bacilli.    There  were  no  typical  granules.    Cultures  are  not  mentioned. 

(4)  Peripleuritis. — Secondary  inflammation  of  the  peripleural  tissue 
is  associated  with  all  pleural  and  many  parapleural  infections.  A 
primary  form  has  been  described,  in  which,  independent  of  neighbor- 
ing disease,  there  is  inflammation  and  suppuration  of  the  tissue  between 
the  costal  pleura  and  the  chest  wall.  Wunderlich,  Billroth,  Bartels, 
Riegel,  and  others  have  described  and  recorded  cases,  but,  as  Martin 
suggests,  with  reliance  on  the  clinical  picture  for  the  establishment 
of  the  group.  Vogel3  has  reported  cases  in  which  at  operation  the 
disease  appeared  to  be  primary.  Idiopathic  peripleuritis  is  rare. 
It  is  usually  localized  and  may  be  acute  or  chronic.  Extension  inward 
is  uncommon,-  while  perforation  of  the  chest  wall  is  frequent.  There 
are  the  usual  symptoms  of  suppuration.  Movement  of  the  affected 
side  may  be  restricted.  The  tissue  overlying  the  inflamed  area 
is  swollen.  The  involved  region  is  dull,  the  breathing  and  fremitus 
diminished  or  absent.  Fluctuation  may  be  established.  The  diag- 
nosis may  be  impossible  before  operation,  and  even  then  it  may  be 
difficult  to  distinguish  between  an  encysted  empyema  and  a  peri- 
pleural abscess.  A  history  of  preceding  pleural  disease  may  suggest 
the  former.  The  absence  of  signs  of  disease  at  the  base  of  the  chest, 
slight  or  failing  dislocation  of  the  heart  and  the  lack  of  shifting  dul- 

1  Jour,  of  Hygiene,  1902,  ii,  120. 

2  Ueber  Miliar-Actinomykose  der  Pleura,  Arbeiten  auf  dem  Gebiete  de  Pathologischen 
Anatomie  und  Bacteriologie,  Baumgarten,  1904,  Bd.  iv,  H.  3. 

»  Dent.  Zeit.  f.  Chir.,  1902-03,  vol.  lxvi. 


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CHRONIC  PLEURITI8  535 

ness  may  distinguish  between  peripleural  abscess  and  ordinary  empy- 
ema, The  prognosis  has  been  regarded  as  unfavorable.  Early  diag- 
nosis followed  by  prompt  and  appropriate  surgical  treatment  may  be 
expected  to  give  favorable  results  in  simple  (non-tuberculous)  and 
uncomplicated  cases. 

(5)  Syphilis  of  the  Pleura. — Cases  of  pleurisy  with  positive  Wasser- 
mann  test  on  the  blood  and  pleural  fluid  have  been  reported  from 
time  to  time.  In  some  instances  negative  inoculation  tests  in  animals 
have  failed  to  show  tuberculosis  in  such  cases,  but  thus  far  the  syphi- 
litic character  of  pleurisy  has  not  been  established. 

(6)  Chronic  Pleuritis. — 1.  Dry  Pleurisy. — This  occurs  as  a  sequel 
to  fibrinous,  serofibrinous,  or  purulent  pleuritis.  Even  in  the  mildest 
cases  of  fibrinous  pleuritis  the  pleura  rarely  escapes  some  damage. 
The  pleura  overlying  a  pulmonary  process  may  be  merely  thickened. 
Adhesions  between  the  pulmonary  and  parietal  layers  are  common. 
On  postmortem  examination  these  may  consist  of  delicate,  thread- 
like connections,  or  as  circumscribed  or  general  synechia?  on  one  or 
both  sides  of  the  chest.  The  lung  may  be  extensively  torn  in  removal 
unless  a  dissection  is  made.  The  pleura  may  reach  a  centimeter  or 
more  in  thickness  and  enclose  single  or  multiple  pockets  of  serous  or 
purulent  fluid.  Deposition  of  lime-salts  may  have  taken  place.  The 
neighboring  lung  is  often  contracted  and  fibrous  in  character.  Bron- 
chiectatic  or  abscess  cavities  are  frequently  found.  The  interstitial 
pulmonary  changes  may  be  due  to  extension  from  the  pleura,  but  it 
is  difficult  in  individual  cases  to  exclude  their  independent  origin. 
The  pleural  changes  may  be  simple  or  tuberculous.  In  the  latter 
instance,  small  tubercles,  fibrocaseous  or  calcified  areas  may  be  found 
in  the  indurated  tissue.  The  site  of  the  process  is  usually  at  the  bases, 
when  it  follows  pleurisy  with  effusion.  In  tuberculous  cases  it  is 
frequently  at  the  apices,  and  extensive  pleural  thickening  may  com- 
plicate slight  pulmonary  infections. 

There  may  be  no  symptoms.  Pain  of  varying  and  usually  slight 
intensity  may  be  present.  Pleuritic  friction  may  exist  without  sub- 
jective symptoms.  Adhesions  usually  prevent  the  rubbing  of  the 
two  pleura?  together,  however,  and  the  signs  are  such  as  have  been 
mentioned  under  Sequela?  in  the  preceding  sections.  Chronic  apical 
pleuritis  may  give  rise  to  depression  of  the  supra-  and  infraclavicular 
fossa?,  to  contraction  of  the  apex,  dulness,  diminished  breathing, 
voice  sounds,  and  tactile  fremitus,  but  coexistent  pulmonary  lesions 
may  make  the  signs  of  thick  pleura  atypical.  An  apical  process  is 
tuberculous  in  a  large  proportion  of  the  cases.  If  pulmonary  tuber- 
culosis is  suspected,  suitable  treatment  should  be  instituted.  In 
non-tuberculous  cases,  with  retraction  of  the  side  and  fixation  of  the 
lung,  pulmonary  gymnastics  may  be  prescribed  to  favor  expansion  and 
improve  the  breathing  capacity. 

2.  Pleurisy  with  Effusion. — In  rare  instances  serofibrinous  or  puru- 
lent fluid  continues  to  reaccumulate  after  repeated  thoracentesis  or 
operation. 


536  DISEASES  OF  THE  PLEURA 

(a)  Serofibrinous  Form.— Persistent  reaccumulatioE  may  be  due  to 
failure  of  the  retracted  and  adherent  lung  to  expand  and  a  neglect 
of  early  tapping  may  be  responsible.  In  some  eases  this  appears  not 
to  be  the  cause,  and  West1  noted  in  two  instances,  with  a  duration  of 
eighteen  months,  that  the  lung  was  still  capable  of  reexpansion. 
In  the  absence  of  malignant  disease  and  obvious  pulmonary  tuber- 
culosis, a  resort  to  operation  may  be  considered  after  other  measures 
have  been  tried.  It  should  be  advised  with  caution,  however,  for  it 
necessarily  induces  empyema,  which  may  also  fail  to  heal,  if  the  lung 
is  adherent. 

(b)  Empyema. — In  this,  as  in  the  serofibrinous  form,  after  pus  has 
remained  long  in  the  chest,  the  lung  may  be  partially  or  wholly  incap- 
able of  reexpansion  from  the  presence  of  abundant  connective- 
tissue  formation  in  and  about  it.  After  operation  and  the  evacuation 
of  pus,  a  space  is  left,  and  in  the  young,  with  less  resistant  thoracic 
walls,  marked  deformity,  retraction  of  the  side,  and  lateral  deviation 
of  the  spine  may  result.  At  times,  from  the  stiffness  of  its  walls, 
the  abscess  cavity  refuses  to  close,  and  cure  can  be  effected  only  by 
more  extensive'  operative  procedures.  In  many  cases  the  first  opera- 
tion has  been  too  long  delayed.  Multiple  costatectomy  (Estlander's 
operation)  may  be  considered  in  persistent  partial,  but  is  not  likely 
to  succeed  in  large  or  total  empyema,  in  the  presence  of  greatly  thick- 
ened parietal  pleura  or  in  old  patients  with  unyielding  thoracic  walls. 
In  such  cases,  Schede's  "  Thoraxresection"  may  be  successful. 

1  Lancet,  March  25,  1905. 


CHAPTER  XXXT. 
HYDROTHORAX. 

Transudation  of  serous  fluid  into  the  pleural  sacs  occurs  in  the 
course  of  many  diseases,  but  when  in  sufficient  amount  to  be  detected 
during  life  is  usully  secondary  to  renal  or  cardiac  disease.  Renal 
disease  gives  rise  to  only  small  amounts  of  pleural  fluid,  but  is  often 
combined  with  cardiac  insufficiency.  Local  stasis  is  probably  a 
contributing  factor  in  connection  with  new-growths  of  the  pleura, 
lung,  or  diaphragm.  Occlusion  of  the  azygos  veins  from  pressure  or 
thrombosis  is  a  possible  cause. 

Cardiac  insufficiency  may  give  rise  to  fluid  in  one  or  both  pleural 
sacs,  with  or  without  general  dropsy.  Cardiac  hydrothorax  is  com- 
monly unilateral  and  right-sided,  and  when  both  pleurae  are  affected 
the  amount  of  fluid  is  usually  greater  on  the  right.  Fetterolf  and 
Landis1  suggest  that  cardiac  hydrothorax  is  due  to  pressure  on  and 
partial  occlusion  of  the  pulmonary  veins  by  dilatated  portions  of 
the  heart.  The  more  common  dilatation  of  the  right  auricle  is  respon- 
sible for  the  greater  frequency  on  the  right.  Of  30  cases  of  cardiac 
hydrothorax  the  effusion  was  bilateral  in  8,  in  6  of  which  the  amount 
of  fluid  was  greater  on  the  right  and  equal  on  the  two  sides  in  the 
remaining  2.  It  was  unilateral  and  right-sided  in  16,  and  confined 
to  the  left  side  in  only  6.  The  predominance  of  right-sided  accumu- 
lations is  too  constant  to  be  accidental  or  to  be  explained  by  previous 
pleuritis  and  obliteration  of  the  left  pleura,  which  can  account  for 
only  a  small  proportion  of  the  cases.  Hydrothorax  from  renal  disease 
alone  is  usually  bilateral.  If,  as  often  happens,  the  heart  is  insuffi- 
cient, the  accumulation  may  be  unilateral  and  right-sided  or  double, 
with  an  excess  on  the  right.  Of  15  cases  in  my  series,  the  effusion 
was  bilateral  in  7,  in  2  of  which  the  amount  was  greater  on  the 
right,  in  3  on  the  left,  and  equal  on  the  two  sides  in  the  remaining  2. 
It  was  unilateral  and  right-sided  in  6,  of  which  5  were  complicated 
by  cardiac  lesions.  The  effusion  was  confined  to  the  left  side  in  2 
cases. 

If  the  decubitus  is  prevailingly  lateral,  a  larger  amount  of  fluid  may 
collect  in  the  dependent  pleura.  The  pleura  may  be  smooth  or  slightly 
clouded  and  swollen.  Old  adhesions  may  limit  the  accumulation 
to  single  or  multiple  pockets.  The  fluid  is  usually  clear  and  yellowish, 
but  may  be  reddish  from  admixture  of  blood.  It  clots  slowly  or  not 
at  all,  and  fibrin  is  absent  in  uncomplicated  cases.    The  specific  gravity 

1  Amer.  Jour.  Med.  Sci.,  1909,  cxxxviii,  712. 


538  DISEASES  OF  THE  PLEURA 

in  venous  transudates  is  usually  from  1010  to  1015,  with  1  to  3  per 
cent,  of  albumin,  while  hydremic  fluids  are  below  1010,  with  traces 
to  1  per  cent,  of  albumin.  The  sediment  usually  shows  an  excess 
of  endothelial  cells.  In  rare  instances  lymphocytes  may  predominate. 
A  complicating  pleuritis  is  not  uncommon,  and  poly  nuclear  cells  may 
then  outnumber  the  other  elements. 

Symptoms. — The  symptoms  are  those  of  the  underlying  disease. 
Pain  is  absent.  If  there  is  fever,  it  cannot  be  ascribed  to  hydrothorax. 
Cough  and  expectoration  may  be  due  to  edema  of  the  lungs.  There 
may  be  gradually  increasing  dyspnea,  which  may  amount  to  orthop- 
nea. The  signs  are  the  same  as  with  pleural  fluid  of  other  character. 
Pleuritic  friction  is  absent.  Shifting  dulness  is  more  readily  obtained. 
Rosenbach  and  Pohl1  find  that  even  small  amounts  of  iodine  or  its 
salts  given  by  mouth  can  be  demonstrated  in  transudates,  but  not 
in  exudates.  The  test  is  performed  by  adding  fuming  nitric  acid  to 
fluid  obtained  by  puncture  and  agitation  with  chloroform,  which  is 
turned  red  if  the  test  is  positive. 

Treatment. — This  is  that  of  the  underlying  disease.  Removal  of 
the  fluid  by  thoracentesis  is  indicated,  if  necessary,  for  the  relief  of 
an  embarrassed  circulation  or  breathing. 

1  Berl.  klin.  Woch.,  1890,  No.  36. 


CHAPTER  XXXII. 
HEMORRHAGIC  PLEURAL  FLUIDS. 

Microscopic  blood  is  always  present  in  pleural  fluids.  Small 
amounts  of  blood  may  arise  from  puncture  of  the  lung  in  thoracentesis. 
Larger  quantities  of  fresh  blood  color  the  fluid  reddish  or  even  blood  red. 
Dieulafoy  estimates  that  5000  to  6000  red  cells  per  c.c.  are  necessary 
to  give  the  fluid  a  definitely  red  color.  Only  cases  with  frankly  hemor- 
rhagic fluid  are  considered  here.  In  old  extravasations  the  fluid  may 
be  reddish-brown,  yellowish,  or  greenish.  Clinically,  it  is  convenient 
to  divide  bloody  fluids  into  hemoserothorax  (hemorrhagic  pleurisy), 
hemohydrothorax,  and  hemothorax. 

(1)  Hemoserothorax  (Hemorrhagic  Pleurisy). — Primary.  —  (a) 
Tuberculous:  An  apparently  primary  disease  of  the  pleura  with 
the  production  of  serohemorrhagic  fluid  is  tuberculous  in  a  great 
majority  of  cases,  (b)  Malignant:  In  a  relatively  small  proportion 
of  cases  it  is  due  to  carcinoma,  rarely  sarcoma.  A  discussion  of  these 
causes  will  be  found  elsewhere.  In  both  groups  it  is  not  infrequently 
observed  that  the  effusion  becomes  more  bloody  with  successive 
tappings,  (c)  Simple  Hemorrhagic  Pleurisy:  There  is  no  sound 
pathologic  evidence  in  support  of  this  group,  as  a  primary  affection, 
although  hemorrhagic  fluids  of  secondary  and  infectious  origin  are 
not  uncommon.  The  clinical  cases  with  an  apparently  primary 
hemoserothorax,  of  simple  origin,  practically  always  run  a  clinical 
course  consistent  with  tuberculosis  or  malignant  disease,  or  show  one 
or  the  other  of  these  conditions  at  autopsy.  There  are  a  few  striking 
exceptions  as  regards  a  more  favorable  clinical  course.  Osier1  refers 
to  a  large,  able-bodied  man,  with  hemorrhagic  exudation,  who  was 
healthy  and  strong  eight  years  afterward.  Cheesman  and  Ely2  reported 
a  most  remarkable  instance  in  a  woman  aged  forty-seven  years,  with 
bloody  fluid  first  in  the  right,  then  in  the  left  chest,  and  finally,  fol- 
lowing the  disappearance  of  this  fluid,  with  bloody  serum  in  the  abdo- 
men. The  pleural  accumulations  continued  for  about  eighteen  months, 
and  no  chest  difficulty  arose  in  the  following  seven  years,  but  in  this 
interval  the  abdomen  was  repeatedly  tapped.  The  abdominal  fluid 
ceased  to  reaccumulate  after  about  five  years,  and  at  the  date  of  the 
report  twenty  months  had  elapsed  without  recurrence.  There  was 
a  large  fibroid  in  the  uterus.  In  all,  two  hundred  and  seventy-nine 
pints  of  fluid  were  removed.3 

1  Prac.  of  Med.,  1905,  p.  651.  2  Amer.  Jour.  Med.  Sci.,  August,  1899. 

3  I  am  informed  that  the  patient  is  entirely  well  twenty-three  years  from  the  onset. 


540  DISEASES  OF  THE  PLEURA 

Secondary. — This  is  a  much  more  common  form.  Cases  due  to 
tuberculosis,  although  they  may  seem  clinically  to  he  primary,  are 
usually  secondary.  So,  also,  in  hemorrhagic  pleurisy  due  to  malignant 
disease,  the  primary  form  is  rare,  that  from  metastasis  relatively 
common,  (uses  not  included  in  these  two  groups  may  he  classed,  as 
in  the  primary  form,  as  simple  hemorrhagic  pleurisy.  Hemorrhagic 
serofibrinous  effusions  of  this  sort  are  perhaps  most  common  in  pneu- 
monia, and  are  usually  due  to  the  pneumoeoccus.  Of  57  cases  of 
croupous  pneumonia,  showing  pleural  effusion  at  autopsy  in  the 
.Massachusetts  General  Hospital,  in  6  the  exudate  was  bloody.  In 
none  of  these  was  there  evidence  of  tuberculosis  of  the  pleura.  An 
inflammation  of  the  pleura  in  the  course  of  malignant  fevers  (variola, 
typhoid)  in  purpura  hemorrhagica  or  complicating  such  asthenic  con- 
ditions as  accompany  malignant  disease,  nephritis,  cirrhosis  of  the 
liver  or  chronic  heart  disease,  may  be  of  the  hemorrhagic  variety, 
whatever  the  cause  of  the  process  in  the  pleura.  Some  prove  to  be 
tuberculosis;  others  are  simple  and  due  to  the  pneumoeoccus  or 
pyogenic  organisms,  the  blood  in  the  exudate  being  due  to  passive 
congestion  or  the  intensity  of  the  local  process. 

An  interesting  feature  of  the  hemorrhagic  pleural  fluids  is  the  high 
percentage  of  eosinophiles  which  they  may  contain  and  the  presence, 
also,  of  a  large  number  of  eosinophiles  in  the  circulating  blood.  In 
Klein's  case1  (autopsy  but  no  microscopic  examination  of  the  tissue) 
the  pleural  fluid  showed  76.4  per  cent,  eosinophiles  (small  lymphocytes, 
23.6  per  cent.),  the  systemic  blood  40  per  cent,  of  eosinophiles.  In 
Harmsen's  case2  the  pleural  fluid  showed  8.64  per  cent,  eosinophiles 
(small  lymphocytes,  87.65  per  cent.).  In  a  case  of  apparently  primary 
disease  of  the  pleura  in  my  series,  the  bloody  pleural  fluid  showed 
no  excess  of  eosinophiles,  but  contained  enormous  numbers  of  choles- 
terin  crj'stals,  while  the  systemic  blood  showed  6400  white  cells,  of 
which  20  per  cent,  were  eosinophiles. 

Hemohydrothorax. — Transudates  may  have  a  hemorrhagic  character 
in  cardiac  or  renal  disease.  Thrombosis  of  the  thoracic  veins  or 
their  occlusion  by  pressure  of  tumors  is  a  possible  cause.  In  Zahn's3 
case  there  was  thrombosis  of  the  azygos  and  intercostal  veins  and 
hemorrhage.  Zahn  was  unable  to  cause  similar  changes  by  experi- 
mental obliteration  of  the  azygos  veins. 

Hemothorax. — This  may  be  due  to  the  rupture  of  intrathoracic 
vessels  following  the  development  of  aneurysm,  their  erosion  by  dis- 
ease or  injury  by  trauma.  In  the  rupture  of  the  aorta  or  its  ulcera- 
tion, the  left  pleura  is  more  often  the  site  of  the  hemorrhage.  The 
pulmonary  veins  and  the  vena  cava  may  rarely  be  the  source.  The 
rupture  of  pulmonary  vessels  from  destructive  pulmonary  processes 
occasionally  leads  to  hemorrhage  into  the  pleural  sac.  The  intercostal 
artieries  may,  likewise,  be  eroded  in  disease  of  the  pleura.    There  is 

1  Cent.  f.  innere  Med.,  January  28    1899.  2  Quoted  from  Klein. 

3  Virchow's  Arehiv,  1885,  p.  345. 


HEMORRHAGIC  PLEURAL  FLUIDS  541 

a  specimen  (No.  2159)  in  the  Warren  Museum  from  a  patient  with 
empyema,  in  whom  erosion  of  an  intercostal  artery  led  to  fatal  hemo- 
thorax.   The  lungs  showed  tuberculosis. 

(2)  Traumatic  Hemothorax. — Etiology. — This  may  arise  from  con- 
tusions of  the  chest,  more  often  from  fracture  of  the  ribs,  and  most 
commonly  from  incised  or  penetrating  wounds.  The  bleeding  may 
come  from  injured  vessels  in  the  thoracic  wall,  more  rarely  from  small 
branches  of  these  parietal  vessels.  Owing  to  the  unprotected  position 
of  the  intercostal  arteries,  their  injury  is  relatively  uncommon.  In 
a  large  proportion  of  cases  the  hemorrhage  is  from  a  wound  of  the 
lung,  superficial  injuries  of  which  may  lead  to  varying  and  usually 
insignificant  hemothorax,  deeper  wounds  to  abundant  hemothorax, 
if  an  important  vessel  is  involved.  The  injury  of  vessels  accompany- 
ing bronchi  of  the  second  or  third  order  may  be  followed  by  hemor- 
rhage compatible  with  survival.1  Wounds  of  vessels  about  the  hilus 
of  the  lung  and  the  larger  mediastinal  vessels  are  followed  by  rapidly 
fatal  hemorrhage. 

Special  Pathology. —  (a)  Onset  of  Hemorrhage. — Following  the  injury 
of  the  larger  bloodvessels,  fatal  hemorrhage  into  the  pleura  may  occur 
within  a  few  minutes.  An  effusion  of  blood  from  the  parietal  vessels 
and  the  lung  usually  begins  at  once  and  is  slowly  continuous.  In  the 
more  favorable  cases  the  bleeding  usually  stops  after  twenty-four  to 
forty-eight  hours.  Delayed  hemorrhage  is  rare.  In  Nelaton's  series 
of  94  cases  a  secondary  and  fatal  hemorrhage  followed  a  gun- 
shot wound  of  the  chest,  in  4  cases,  on  the  second,  the  tenth,  the 
twelfth,  and  the  thirty-sixth  day  respectively.  In  Vaille  and  Braun's 
case,  following  a  knife  cut  in  the  second  left  intercostal  space,  hemo- 
thorax due  to  the  rupture  of  a  traumatic  aneurysm  of  the  internal 
mammary  artery  occurred  on  the  nineteenth  day. 

(b)  Time  of  Coagulation. — In  experimental  work  the  introduction 
of  artificial  conditions  limits  the  value  of  the  observations.  Nelaton 
caused  hemothorax  in  animals  by  injuring  the  lung  with  a  knife,  and 
found  that  the  extravasated  blood  coagulated  within  twenty-four 
hours,  as  shown  by  autopsy.  His  experiments  were  not  performed 
under  aseptic  precautions.  Penzolt2  found,  in  fourteen  experiments, 
that  the  blood  at  first  remains  fluid,  that  large  effusions  coagulate 
after  two  hours,  and  that  small  amounts  of  blood  coagulate  at  the  latest 
after  twenty-four  hours.  Pagenstecher3  found,  in  nine  experiments, 
that  blood  injected  into  the  pleural  cavity  is  still  fluid  after  about 
two  hours,  while  clots  and  uncoagulated  fluid  are  present  after  about 
six  hours.  The  reports  of  surgical  interference  and  the  autopsy  table, 
although  not  numerous,  suggest  that  coagulation  of  the  effused 
blood  invariably  occurs  in  man  and  probably  within  an  equal  period. 
It  is  frequently  noted  that  hemorrhagic  pleural  fluid  does  not  coagu- 

1  Nelaton,  "Des  epanchements  de  sang  dans  les  plevres,  etc.,"  These  de  Paris,  1880. 

2  Deut.  Arch.  f.  klin.  Med.,  1876,  p.  542. 

3  Beitrage  zur  klinischen  Chirurgie,  Tubingen,  1895,  xiii,  264. 


542  DISEASES  OF   THE  PLEURA 

[ate  on  removal,  and  this  is  probably  due  to  its  previous  coagulation 
within  the  chest. 

(c)  Absorption, — In. favorable  and  uncomplicated  cases  the  fluid 
is  wholly  absorbed.  The  blood  clot  becomes  adherent  to  the  pleural 
surfaces,  softening  and  organization  take  place,  and  after  small  extrav- 
asations, nothing  but  a  few  adhesions  may  remain.  With  large 
hemorrhages  and  much  clot,  more  extensive  adhesions  and  thickening 
of  the  pleura  persist.  The  affected  side  may  show  diminished  expan- 
sion. 

(d)  Occurrence  of  Pleuritis. — The  blood  is  not  in  itself  a  cause  of 
pleuritis,  and  when  infection  occurs  in  hemothorax,  it  is  due  to  bac- 
teria which  have  invaded  the  pleural  sac  from  without,  through  the 
thoracic  wound  or  the  lung.  The  incidence  of  suppuration  in  traumatic 
hemothorax  is  uncertain,  from  the  lack  of  any  series  of  unselected 
cases  of  sufficient  number  dealing  with  this  point.  Its  occurrence  can, 
therefore,  be  formulated  only  in  a  general  way.  It  is  less  frequent  in 
small  effusions,  and  is  less  likely  to  occur  following  injuries  of  the 
parietal  vessels  or  the  superficial  parts  of  the  lung,  without  an  external 
wound.  Large  effusions  of  blood,  those  arising  from  incised  or  pene- 
trating wounds,  and  hemorrhage  from  the  deeper  parts  of  the  lung, 
often  become  purulent. 

(e)  Examination  of  the  Pleural  Fluid  Obtained  by  Puncture. — Obser- 
vations are  rare  on  this  point.  The  number  of  red  cells  progressively 
diminishes  in  the  effused  blood.  This  is  partly  due  to  the  dissolution 
of  red  cells  in  the  fluid,  to  phagocytosis  by  endothelial  cells,  and  to 
sedimentation,  counts  in  fluid  taken  from  different  levels  showing 
fewer  reds  and  a  larger  number  of  white  cells  above,  while  the  opposite 
is  true  below.  In  judging  the  presence  of  an  infection  from  an  enumera- 
tion and  differential  count  of  the  white  cells,  due  allowance  must  be 
made  for  the  number  of  polynuclear  cells  in  the  effused  blood.  In 
De  Gery  and  Froin's  case  of  traumatic  hemothorax,  a  differential 
count  of  the  white  cells  in  the  effused  blood  showed:  large  mono- 
nuclear cells,  90.42  per  cent.;  lymphocytes,  2.12  per  cent.;  poly- 
nuclears,  3.72  per  cent.;  eosinophils,  3.72  per  cent.  Three  days 
later  the  eosinophiles  numbered  28.76  per  cent.  In  Harmsen's  case 
there  was  a  marked  systemic  leukocytosis  with  eosinophiles  in  both 
systemic  and  pleural  blood. 

(/)  Relation  to  Tuberculosis. — Hemorrhagic  pleural  effusion  fol- 
lowing trauma  may  rarely  be  tuberculous.  Lustig1  relates  the  case 
of  a  laborer,  aged  forty-three  years,  with  tuberculous  antecedents,  in 
whom  a  left-sided  hemorrhagic  effusion  followed  a  fall,  in  which  the 
left  chest  struck  against  a  wheel.  Death  occurred  one  month  later. 
Autopsy  showed  tuberculosis  of  the  left  pleura. 

Symptoms. — In  small  and  slowly  accumulating  effusions  there  may 
be  no  symptoms.     Shock  is  a  variable  feature.     Pressure  symptoms 

1  Quoted  from  Trouve,  These  de  Paris,  1902. 


PLATE   II 


Pyopneumothorax — Right   Side.     (James. 


Pyopneumothorax — Left  Side.     (James.) 


HEMORRHAGIC  PLEURAL  FLUIDS  543 

usually  occur  within  twenty-four  hours  and  are  rarely  delayed  for 
forty-eight  hours.  In  one  of  Nelaton's  cases  the  hemorrhage  was 
delayed  for  thirty-six  days.  With  the  rapid  accumulation  of  a  large 
amount  of  blood,  death  may  ensue  within  a  few  minutes.  In  most 
cases  there  is  slowly  increasing  dyspnea,  which  is  the  most  constant 
symptom,  due  to  collapse  of  the  lung  and  consequent  dislocation  of 
the  mediastinum.  Pain  may  be  present,  and  is  usually  referred  to  the 
affected  side.  Cough  is  an  inconstant  symptom.  If  the  lung  is 
wounded  there  is  likely  to  be  hemoptysis.  Blood  in  the  sputum  may 
consist  of  blood  streaks,  or  there  may  be  frank  hemoptysis'.  In  addi- 
tion, with  the  more  rapid  accumulation,  there  are  symptoms  due  to  loss 
of  blood,  pallor,  progressive  elevation  of  the  pulse,  with  alteration  in 
its  quality,  coldness  of  the  extremities  and  body,  and  sweating.  Syn- 
cope or  delirium  may  occur.  The  temperature  may  be  subnormal 
at  first,  and  in  favorable  cases  may  not  exceed  normal  limits.  In  a 
considerable  proportion  of  cases  the  temperature  rises,  after  the  first 
or  second  day,  a  degree,  a  degree  and  a  half,  or  even  two  degrees 
Fahrenheit,  and  remains  thus  elevated  for  several  days.  Although 
such  an  elevation  of  temperature  naturally  occasions  much  anxiety, 
such  cases  not  infrequently  progress  favorably.  The  rise  in  tempera- 
ture may  be  due  to  absorption.  The  physical  signs  differ  in  no  respect 
from  those  with  pleural  fluids  of  other  character. 

Complications  and  Sequelae. — Infection  of  the  effused  blood  is  most 
to  be  feared.  There  are  no  trustworthy  statistics  concerning  the  fre- 
quency with  which  empyema  develops,  but  it  appears  from  Nelaton's 
94  collected  cases  that  the  effusion  became  purulent  with  more  or  less 
certainty  in  21.  Hemopneumothorax  is  common,  and  may  become 
pyopneumohemothorax.  Pneumonia,  pulmonary  abscess,  or  gangrene 
may  arise  from  the  injury  or  follow  as  a  result  of  neglected  empyema. 
The  rupture  of  traumatic  aneurysm  of  the  internal  mammary  artery 
was  the  apparent  cause  of  hemothorax,  which  developed  nineteen 
days  after  the  injury  in  Vialle  and  Braun's  case.  Recovery  followed 
ligation  of  this  artery.  An  unruptured  aneurysm  of  the  same  artery 
was  found  after  death  in  DeMontegre's  case.  In  both  there  was 
localized  pulsating  tumor,  and  in  the  former  a  systolic  murmur. 

Diagnosis. — A  careful  physical  examination  should  be  made  when 
the  patient  first  comes  under  observation.  A  neglect  of  this  precau- 
tion may  lead  to  unnecessary  delay  in  the  diagnosis  of  an  empyema. 
A  pleural  effusion  developing  within  a  few  hours  of  a  thoracic  injury 
means  hemothorax  with  practical  certainty;  a  delayed  effusion  is 
usually  inflammatory,  rarely  hemorrhagic.  The  early  detection  of 
infection  is  most  important.  Evidence  of  its  occurrence  is  usually 
afforded  by  elevation  of  temperature,  which  commonly  takes  place 
from  the  third  to  the  fifth  day,  and  is  accompanied  by  other  symptoms 
of  sepsis,  such  as  are  ordinarily  seen  in  empyema.  Symptoms  of 
sepsis  may  develop,  however,  only  after  days  or  weeks  have  elapsed. 
The  presence  of  an  infection  may  be  suspected  when,  even  without 


.".I!  DISEASES  OF   THE  PLEURA 

fever,  there  is  a  delay  in  the  absorption  of  the  fluid,  which  in  most 
cases  progressively  diminishes  in  amount,  and  moderate  effusions 
may  be  fully  absorbed  within  a  month.  Any  increase  of  a  fluid  which 
has  previously  reached  a  standstill  should  likewise  be  regarded  as  due 
to  inflammation  and  not  recurrent  hemorrhage,  which  is  relatively 
uncommon.  An  enumeration  at  intervals  of  the  white  cells  in  the 
systemic  blood  may  be  of  value  in  the  early  recognition  of  suppura- 
tion.    An  initial  leukocytosis  may  be  due  to  hemorrhage  alone. 

Exploratory  puncture  and  the  withdrawal  of  sufficient  fluid  for 
diagnosis  should  be  done  if  empyema  is  suspected.  If  the  puncture 
is  made  at  a  distance  from  the  original  injury  there  is  less  danger  of 
dislodging  an  occluding  thrombus.  The  needle  should  be  inserted 
toward  the  upper  rather  than  the  lower  level  of  the  fluid,  to  avoid  a 
dry  tap  from  penetration  of  the  clot.  If  properly  performed,  and 
under  rigidly  aseptic  precautions,  the  procedure  is  practically  devoid 
of  danger.  An  infection  may  be  sufficiently  obvious  from  inspection 
of  the  fluid.  In  developing  or  mild  infections  microscopic  examination 
of  the  sediment  may  show  an  excess  of  polynuclear  cells  and  also  that 
degenerative  processes  are  at  work,  from  their  necrotic  appearance. 
(  ultures  should  be  taken. 

Prognosis. — Traumatic  hemothorax  is  always  serious.  The  site, 
extent,  and  character  of  the  original  injury,  the  rapidity  with  which 
the  hemorrhage  takes  place  and  the  amount  of  effused  blood  are  impor- 
tant factors.  In  some  cases  the  effusion  may  be  small,  and  pneumo- 
thorax may  be  the  significant  feature.  To  these  dangers  that  of 
infection  is  added.  Of  Nekton's  94  cases  of  traumatic  hemothorax, 
gathered  from  the  older  literature,  49  died  from  immediate  or  remote 
causes.  The  seriousness  of  chest  injuries,  in  general,  can  be  gathered 
from  the  cases  collected  from  the  literature  by  Garre.1  In  37  cases 
of  pulmonary  rupture  the  mortality  was  63  per  cent.;  in  100  cases  of 
punctured  wounds,  38  per  cent.;  in  535  bullet  wounds,  30  per  cent. 
Hemorrhage,  pneumothorax,  or  infection  are  the  principal  causes  of 
death. 

Treatment. — The  cases  come  within  the  province  of  the  surgeon. 
Aside  from  the  surgical  care  of  external  wounds  an  expectant  policy 
should  be  followed  in  cases  without  alarming  symptoms.  The  patient 
should  be  absolutely  at  rest.  Immobilization  of  the  affected  side  by 
strips  of  adhesive  plaster  may  favor  cessation  of  the  hemorrhage.  The 
administration  of  lactate  of  calcium,  15  gr.  (1  gram),  four  times  a  day, 
may  be  of  value.  The  hemothorax  if  uninfected  will  be  absorbed.  If 
suppuration  occurs,  the  empyema  should  be  opened  and  drained. 
The  large  proportion  of  deaths  from  hemorrhage,  from  suffocation 
by  hemothorax  or  pneumothorax,  and  the  frequency  with  which  the 
pleura  becomes  infected,  leaves  much  to  be  desired  from  surgery  in 
the  care  of  such  cases. 

1  Archiv  f.  klin.  Chir.,  1905,  lxxvii,  209. 


HEMORRHAGIC  PLEURAL  FLUIDS  545 

Although  the  cleaning  and  disinfection  of  external  wounds  may  be 
secured,  and  doubtless  eliminates  a  small  measure  of  infection,  there 
still  remains  the  considerable  danger  of  infected  material  already 
carried  into  the  thorax  or  arising  in  consequence  of  a  communication 
between  the  lung  and  the  pleura.  In  cases  with  alarming  symptoms, 
as  a  life-saving  measure,  a  more  active  surgical  intervention  may 
properly  be  considered.  A  source  of  the  hemorrhage  in  a  parietal 
vessel  may  at  times  be  determined  from  the  site  of  the  injury.  The 
lung  itself  is,  however,  more  often  the  source,  and  then  surgery  is  less 
likely  to  be  successful.  The  lung  is  likely  to  be  partly  or  wholly  col- 
lapsed and  the  bleeding  wound  difficult  to  find  or  to  reach.  Suture  of 
the  lung  has  as  yet  been  too  infrequently  performed  to  furnish  trust- 
worthy statistics. 

Thoracentesis  and  the  slow  withdrawal  of  blood  has  been  advised, 
for  the  most  part  by  French  surgeons,  for  alarming  pressure  symptoms 
following  hemothorax.  Bourgeois1  was  able  to  collect  9  cases  in  which 
thoracentesis  was  performed  on  the  first  to  the  fourth  day,  with  recov- 
ery. No  unfavorable  cases  are  mentioned.  The  measure  is  regarded 
not  only  as  palliative,  but  also  as  curative,  on  the  theory  that  the 
collapsed  lung  is  congested  and  thus  bleeds  more  readily  than  other- 
wise. In  cases  obviously  suffering  from  pressure  and  without  marked 
symptoms  of  hemorrhage,  the  procedure  may  be  tried. 


1  "Traitement  par  la  ponction  de  l'hemothorax  traumatique,"   Thdse,   Lyon, 


1905. 


35 


CHAPTER  XXXIII. 
CHYLOTHORAX. 

Chylous  and  Chyliform  Pleural  Fluids.— Much  confusion  exists 
in  the  classification  of  milky  fluids  which  may  accumulate  in  the 
serous  sacs.  Quincke,1  in  1875,  grouped  the  cases  into  those  with 
chylous  fluid  (hydrops  chylosus)  in  which  the  appearance  was  due 
to  the  presence  of  true  chyle,  and  a  second  class  with  fluid  of  a  chylous 
appearance  (hydrops  chyliformis  seu  adiposus),  the  milky  character 
being  due  to  cells  undergoing  fatty  degeneration.  The  distinction 
is  often  difficult  and  at  times  impossible.  The  two  types  of  fluid  may 
be  present  in  different  cases,  both  of  which  are  due  to  a  similar  cause, 
and  a  single  sample  of  fluid  may  likewise  present  features  common 
to  both  forms.  The  differentiation  from  the  presence  of  sugar,  which, 
in  more  than  questionable  traces,  Senator2  regarded  as  an  indication  of 
the  chylous  nature  of  the  fluid,  cannot  be  relied  upon,  since  Rotmann3 
showed  that  serous  fluids  (without  chyle)  may  also  contain  from 
0.055  to  0.112  per  cent,  of  sugar.  Rotmann  believes  that  sugar  is 
a  differential  sign  of  importance  only  when  present  in  an  amount 
exceeding  0.2  per  cent. 

Such  fluids  are  white  and  milky  in  appearance,  but  may  be  reddish 
from  the  presence  of  blood  or  show  varying  shades  of  yellow  or  green. 
In  the  last  instance  they  may  readily  be  mistaken  for  purulent  fluid. 
They  are  usually  colorless,  but  may  be  slightly  sweetish.  Thin  layers 
are  opalescent.  On  standing,  a  creamy  layer  of  fat  collects  at  the 
surface.  They  are  resistant  against  putrefaction.  Their  milky 
appearance  is  maintained  after  filtration  or  centrifugalization,  but 
they  can  be  cleared  by  shaking  with  ether.  From  0.06  to  3.71  per 
cent,  of  fat  has  been  extracted.  The  amount  of  albumin  is  variable; 
from  3.36  to  7.37  per  cent,  has  been  reported,  with  traces  of  casein 
in  one  instance.  Solids  are  present  from  5  to  10  per  cent.,  inorganic 
substances  (salts  and  extractives)  about  1  per  cent.  Fibrin  is  variable, 
present  in  some,  absent  in  other  cases.  Cholesterin,  lecithin,  cal- 
cium, magnesium,  potassium,  sodium,  chlorin,  and  carbonic,  sul- 
phuric, and  phosphoric  acids  have  been  found.  Microscopic  examina- 
tion discloses  a  large  number  of  minute  fat  droplets  about  the  size 
of  micrococci,  but  readily  differentiated  from  microorganisms.  In 
the  chylous  fluids  the  fat  granules  are  very  numerous,  with  only  few 
formed  elements,  while  the  chyliform  fluids  contain  less  numerous 

1  Deut.  Arch.  f.  klin.  Med.,  Bd.  xvi,  pp.  121  to  139. 

-  Charite-Annalen,  vol.  xx,  p.  253.  3  Zeit.  f.  klin.  Med.,  1896,  xxxi,  416. 


CHYLOTHORAX  547 

fat  granules,  of  larger  size,  and  more  numerous  cells  in  different  stages 
of  fatty  degeneration. 

Pseudochylous  Fluids. — Pleural  fluid  without  fat  may  have  a  milky 
appearance.  Quincke  showed  that  albumin  in  fine  subdivision  may 
cause  a  milky  appearance.  Lion,1  in  1893,  showed  that  fat  was  absent 
in  a  milky  abdominal  fluid  which  he  studied.  An  albuminous  body 
was  found,  the  nature  of  which  was  uncertain.  Such  substances  have 
been  regarded  as  lecithin,  globulin,  casein,  or  a  compound  of  globulin 
and  lecithin.  These  pseudochylous  fluids  are  distinguished  from  the 
chylous  and  chyliform  fluids  by  the  separation  of  the  latter  into  two 
layers  on  standing,  while  the  former  remain  homogeneous.  The 
microscopic  examination  of  chylous  or  chyliform  fluids  shows  the 
presence  of  fat,  which  may  be  stained  black  with  osmic  acid  or  removed 
by  shaking  with  ether.  In  gross  appearance  chylous  and  chyliform 
fluids  may  resemble  purulent  fluids,  from  which  they  can  be  differ- 
entiated by  more  careful  examination. 

Occurrence. — Chylous  or  chyliform  pleural  fluids  are  of  infrequent 
occurrence.  It  is  probable  that  they  are  more  common,  however, 
than  the  number  of  reported  cases  indicates,  since  chylous  may  be 
readily  confused  with  purulent  fluid,  unless  carefully  examined. 
Bargebuhr2  was  able  to  collect  41  cases,  reported  from  1633  to  1894, 
an  incidence  of  1  case  reported  about  every  six  years.  Rotmann  in 
1896  brought  the  number  to  49. 

Etiology. — Of  40  cases  in  Rotmann's  series,  in  which  the  cause  could 
be  determined,  27  were  classed  as  chylous,  13  as  chyliform.  Of  the 
chylous  cases,  8  were  due  to  trauma;  5  to  cancer  of  the  pleura;  4  to 
occlusion  of  the  left  subclavian  vein.  Two  cases  were  ascribed  to  each 
of  the  following  causes :  compression  of  the  duct  by  tumors,  disease 
of  the  lymph  vessels  (sclerosis,  lymphangiectasis) ,  and  malignant 
lymphoma,  and  1  case  to  each  condition  as  follows:  occlusion  of  the 
thoracic  duct,  excessive  exertion  and  parasites  (filaria?).  The  pres- 
ence of  chyliform  fluid,  with  admixture  of  fatty  degenerated  cells,  was 
due  to  cancer  of  the  pleura,  lymph  vessels,  etc.,  in  5;  tuberculous 
pleuritis  in  3;  exudative  (non-tuberculous)  pleuritis  in  3;  and  pul- 
monary abscess  (?)  in  1.  One  case  was  regarded  as  the  result  of  an 
abnormal  amount  of  fat  in  the  blood  (lipemia?). 

Diagnosis. — The  chylous  or  chyliform  character  of  a  pleural  fluid 
can  be  determined  with  certainty  only  by  an  examination  of  the  fluid. 
Its  presence  may  be  suspected,  however,  following  trauma,  with  malig- 
nant disease  of  the  pleura,  glands,  or  lymphatics,  and  with  throm- 
bosis of  the  left  subclavian  vein.  The  association  of  pleural  fluid  with 
the  known  presence  of  chylous  ascites  may  suggest  a  chylous  char- 
acter to  the  former.  Uncomplicated  cases  of  chylous  or  chyliform 
pleural  fluid  are  usually  afebrile.  Such  an  accumulation  may  occur 
at  any  age  and  in  either  or  both  pleural  sacs. 

1  Archiv  de  med.  experiment.,  1893,  No.  6,  p.  826. 

2  Deut.  Arch.  f.  klin.  Med.,  1895,  vol.  liv. 


548  DISEASES  OF  THE  PLEURA 

Prognosis.  —Chylous  Fluids. — The  transudation  of  chyle  into  the 
pleura  adds  to  the  danger  of  the  underlying  disease,  the  additional 
tax  on  the  patient  from  the  loss  of  food  which  would  otherwise  be 
utilized  in  the  system.  Thus  the  course  of  an  affection  steadily  pro- 
gressing toward  a  fatal  termination  may  be  hastened.  The  rapidity 
and  extent  of  the  accumulation  are  important  for  the  estimation  of  its 
effect  on  the  patient.  Small  accumulations,  the  removal  of  which  is 
unnecessary,  probably  add  little  to  the  danger  of  the  original  disease. 
The  prognosis  becomes  more  unfavorable  when  the  frequent  recur- 
rence of  alarming  pressure  symptoms  necessitates  the  repeated  with- 
drawal of  large  amounts  of  chylous  fluid.  The  underlying  cause  is 
usually  of  so  grave  a  nature  that  in  general  the  prognosis  must  be 
considered  unfavorable.  Of  22  cases  (11  classed  as  chylous,  11  prob- 
ably chylous)  in  Rotmann's  series  only  4  recovered.  Of  these,  2  were 
due  to  trauma,  1  to  probable  disease  of  the  lymph  vessels,  and  the 
last  to  an  uncertain  cause. 

Chyliform  Fluids'. — The  prognosis  in  cases  with  chyliform  pleural 
fluid  is  more  nearly  that  of  the  underlying  cause,  such  cases  being 
due  to  the  fatty  degeneration  of  existing  cells. 

In  cases  with  chylothorax  in  which  recovery  has  followed,  it  is  prob- 
able that  the  chylous  transudation  has  come  from  branches  of  the 
main  thoracic  duct  or  that  the  occlusion  of  the  latter  is  compensated 
by  an  abundant  collateral  circulation.  Slight  lesions  of  the  thoracic 
duct  may  heal  and  the  duct  remain  patent. 

Traumatic  Chylothorax. — Such  cases  present  features  of  special 
interest  from  their  rarity  and  more  favorable  prognosis.  Of  11  cases, 
recorded  in  the  literature,  the  chylothorax  was  double  in  1  case  (Hens- 
sen),  left-sided  with  right  hemothorax  in  1  (Handmann's  first  case), 
right-sided  with  left  pneumothorax  in  1  (v.  Thaden),  and  confined 
to  the  right  side  in  the  remaining  8  cases  (Quincke,  Kirschner,  Krabbel, 
Helferich,  Handmann,  Hahn,  Dietze,  and  Lindstrom).  The  traumatic 
cases  may  be  fatal  from  the  original  injury  plus  the  mechanical  effect 
of  the  pleural  fluid,  or  in  time  from  loss  of  lymph. 

In  1  of  the  reported  cases  (Dietze)  an  injury  to  the  thoracic  duct 
followed  a  self-inflicted  bullet  wound.  In  the  remaining  cases  the 
chylothorax  was  due  to  severe  mechanical  injury  to  the  thorax,  with 
certain  or  probable  fracture  of  the  ribs.  In  2  of  the  5  fatal  cases  the 
thoracic  duct  was  found  to  have  been  injured  by  fragments  of  the 
tenth  and  eleventh  dorsal  vertebra?  respectively.  The  mechanism 
of  the  injury  to  the  duct  in  the  other  cases  is  uncertain.  It  may  have 
been  lacerated  or  ruptured  by  bony  fragments  of  the  ribs  or  vertebras, 
or  compressed  between  the  mediastinal  structures  and  the  vertebral 
bodies  with  sufficient  force  to  injure  it,  without  injury  to  the  more 
resistant  neighboring  structures  (aorta,  azygos  vein,  esophagus). 
In  these  cases  the  implication  of  the  parietal  pleura  in  the  injured 
structures  is  indicated  by  the  presence  of  chylous  fluid  in  the  pleural 
sac.    Rupture  of  the  thoracic  duct  may,  however,  lead  to  an  accumu- 


CHYLOTHORAX  549 

lation  of  chyle  outside  the  pleural  sac  provided  the  parietal  pleura  is 
uninjured.  Under  these  circumstances  the  mediastinum  may  he 
infiltrated  or  the  parietal  pleura  dissected  up  from  the  thoracic  wall, 
as  in  Eyer's  case. 

Treatment. — This  presents  a  somewhat  different  problem  from  other 
pleural  fluid,  since  the  diminution  of  pleural  pressure  favors  reaccumu- 
lation  and  changes  in  pressure  interfere  with  the  healing  of  lesions 
of  the  lymphatic  vessels.  The  repeated  loss  of  large  amounts  of  such 
fluid  is  a  severe  drain,  It  is  best,  therefore,  in  the  presence  of  small 
amounts  of  fluid  to  keep  the  patient  under  observation  after  suffi- 
cient material  has  been  withdrawn  for  diagnostic  purposes.  Strapping 
the  affected  side  may  prevent  an  increase  of  the  fluid  by  diminishing 
the  respiratory  changes  in  intrapleural  tension.  In  the  traumatic 
cases  an  expectant  policy  was  followed  by  spontaneous  absorption 
of  the  fluid  in  two  instances  (cases  of  Henssen  and  Handmann). 
When  an  excessive  amount  of  fluid  has  accumulated  it  must  be  evacu- 
ated with  the  trocar.  This  was  done  in  6  cases,  with  3  deaths  (cases 
of  Quincke,  v.  Thaden,  and  Hahn)  and  3  recoveries  (cases  of  Kirsch- 
ner,  Handmann's  second  case,  and  Dietze).  In  Hahn's  fatal  case, 
twenty-nine  liters  of  fluid  were  removed  within  twenty-six  days. 
Dietze's  patient  recovered  after  the  withdrawal  of  twenty-seven  liters 
in  thirty-one  days.  If  possible,  operation  should  be  delayed  until 
the  level  of  the  fluid  has  ceased  to  rise.  It  is  better  to  remove  small 
amounts  frequently  than  a  large  amount  at  one  time.  In  1  case 
(Krabbel)  the  fluid,  six  liters  in  amount,  was  first  discovered  at  autopsy. 
Because  of  the  inaccessible  site  of  the  thoracic  duct  an  attempt  at 
its  ligation  is  hardly  likely  to  prove  successful.  An  increase  of  intra- 
pleural pressure  to  that  of  the  atmosphere,  following  resection  of  a 
rib,  may  effect  a  cure.  Thoracotomy  was  followed  by  recovery  in  one 
case  (Helferich)  and  death  in  another  (Lindstrom). 


CHAPTER  XXXIV. 
TUMORS   OF  THE   PLEURA. 

BENIGN  TUMORS. 

These  are  rare  and  without  a  distinctive  clinical  picture.  They 
usually  run  their  course  undetected  during  life,  and  are  first  dis- 
covered at  autopsy.  In  general  they  consist  of  tumors  arising  in 
neighboring  organs  which  invade  the  pleura  by  encroachment,  usually 
remaining  extrapleural,  at  times  projecting  into  the  pleural  space, 
but  enveloped  by  its  visceral  or  parietal  layer. 

Aberrant  lung  tissue  may  project  into  the  pleural  space.  In  a  case 
described  by  Muus,1  a  smooth  tumor  the  size  of  a  walnut  was  found 
in  the  left  pleural  cavity,  attached  to  the  diaphragm  and  covered  by 
diaphragmatic  pleura.  The  tumor  showed  on  section  an  alveolar 
arrangement.  The  alveolar  septa  contained  vessels  and  fine  muscle 
fibrilla?.  Connective  tissue,  cartilage,  elastic  fibers,  and  ciliated  cylin- 
drical epithelium  were  also  present.  Small  single  or  multiple  cysts 
of  the  pleura  are  described  by  Stilling2  and  Zahn.3  Their  walls  con- 
tained cartilage  and  acinous  glands,  lined  with  ciliated  epithelium, 
suggesting  their  origin  from  the  bronchi.  Emphysema  may  give  rise 
to  cyst-like  structures  projecting  into  the  pleural  cavity  (bullous 
marginal  emphysema).  A  specimen  in  the  Warren  Museum  (No. 
2142)  shows  such  a  bleb,  the  size  of  a  horse-chestnut,  its  walls  com- 
posed of  thickened  pulmonary  pleura,  lined  with  delicate  trabecular 
and  connecting  with  the  bronchi.  They  may  reach  a  much  larger 
size.  Their  rupture  may  give  rise  to  pneumothorax.  Pulmonary 
adenoma,  angioma,  or  osteoma  may  invade  the  pleural  sac.  Fibroma 
may  arise  in  the  lung  and  similarly  invade  the  pleura. 

Lipoma. — Fatty  tumors  may  in  rare  instances  arise  from  the  subpleural 
fatty  tissue  and  project  into  the  pleural  sac.  They  are  usually  too  small 
to  give  rise  to  symptoms  or  physical  signs,  and  are  discovered  post- 
mortem, growing  from  the  costal,  diaphragmatic,  or  mediastinal  fatty 
tissue  as  rounded  or  flattened,  sessile  or  pedunculated  masses.  F'itz4 
reviewed  the  literature  and  reported  a  case.  In  rare  instances,  lipoma 
of  the  thoracic  wall  may  communicate  with  the  subpleural  space  and 
project  into  the  pleural  sac,  as  in  the  cases  of  Czerny,5  Plettner,6 

1  Virchow's  Archiv,  vol.  clxxvi,  p.  180.  2  Ibid.,  Bd.  cxiv,  p.  557. 

3  Ibid.,  vol.  cxliii,  pp.  173  and  416. 

4  Trans.  Assoc.  Amer.  Phys.,  1905,  vol.  xx. 

6  Wien.  med.  Woch.,  1875,  xxv,  166.  G  Inaug.  Diss.,  Halle,  1889. 


TUMORS  OF  THE  PLEURA  551 

Gussenbauer,1  and  Kronlein.2  Such  possible  communication  through 
the  thoracic  wall  with  the  thoracic  cavity  should  be  borne  in  mind 
in  operations  for  the  removal  of  subcutaneous  lipomas,  as  infection 
of  the  wound  may  readily  lead  to  infection  of  the  pleura.  In  Kron- 
lein's  case,  a  female  infant  aged  one  year,  a  lipoma  occupied  a  large  part 
of  the  front  of  the  right  chest;  at  operation  it  was  found  to  be  con- 
tinuous by  a  pedicle  the  size  of  the  thumb,  passing  through  the  third 
interspace  1  cm.  from  the  right  sternal  margin,  with  a  similar  growth, 
as  large  as  a  child's  head,  almost  entirely  filling  the  anterolateral 
portion  of  the  left  thoracic  cavity.  In  Fitz's  case  a  lipoma  about  the 
size  of  a  newborn  child's  head  was  found  at  autopsy  in  the  inferior 
and  lateral  portion  of  the  left  pleural  cavity  and  apparently  con- 
tinuous with  the  fat  tissue  of  the  superior  mediastinum.  It  was 
apparently  covered  by  the  pleura,  and  was  adherent  to  the  diaphragm, 
pericardium,  and  parietal  pleura.  The  mass  obscured  an  acute 
purulent  pericarditis  arising  in  the  course  of  lobar  pneumonia. 


PRIMARY  MALIGNANT  TUMORS. 

Carcinoma. — Synonyms. — Endothelioma ;  endothelioma  lymphangio- 
matosum;  pleuritis  carcinosa;  lymphangitis  carcinomatodes;  lym- 
phangitis prolif era ;  sarcocarcinoma.  Although  the  term  endothelioma 
has  been  most  commonly  applied,  carcinoma  seems  more  appropriate. 
The  general  character  and  histologic  appearance  of  the  tumor  do 
not,  in  general,  sufficiently  differ  from  carcinoma  in  other  regions,  and 
its  origin  in  the  surface  epithelium  or  lymphvessel  endothelium  is  too 
uncertain  to  warrant  a  more  distinctive  term. 

Occurrence. — This  is  a  rare  affection,  of  which  some  40  to  50  cases 
are  sufficiently  well  recorded  to  permit  of  acceptance.3  I  have  had 
the  opportunity  of  studying  sections  from  3  cases.  It  is  probable 
that  the  condition  has  not  infrequently  escaped  detection  because 
of  the  readiness  with  which  it  may  be  confused  with  chronic  pleuritis, 
without  a  microscopic  examination  of  the  tissue.  The  disease  is  more 
common  between  forty  and  fifty  years,  but  the  ages  of  the  reported 
cases  vary  from  ten  to  seventy-four  years.  Men  are  somewhat  more 
frequently  affected.  In  rare  instances.it  has  followed  trauma  to  the 
chest  wall. 

Pathology. — The  disease  is  usually  unilateral  and  occurs  about 
equally  on  the  two  sides,  although  the  right  pleura  has  been  somewhat 
more  commonly  involved.  Rarely  both  pleurae  are  invaded.  The 
entire  pleura  of  one  side  may  be  increased  in  thickness  to  1,  1.5,  or 
even  to  2  cm.    In  other  cases  only  a  part  of  the  pleural  sac  is  diseased. 

1  Arch.  f.  klin.  Chir.,  1892,  xliii,  322.  2  Ibid.,  1877,  xxi,  Suppl.,  157. 

3  Cases  reported  to  1897  have  been  collected  by  Glockner,  Zeit.  f.  Heilkunde,  1897, 
vol.  xviii;  to  1905  by  Bloch,  Les  Neoplasmes  malms  primitifs  de  la  plevre,  Paris,  Vigot 
Freres. 


552  DISEASES   OF    THE    PLEURA 

The  affected  region  is  usually  diffusely  invaded,  is  gray  or  grayish- 
yellow  in  color,  and  studded  with  discrete  or  confluent  white,  grayish 
or  yellowish  nodnlcs,  varying  in  si/A-  from  a  pinhead  to  a  pea.  More 
rarely  the  pleura  is  the  site  of  larger,  multiple  and  isolated  masses  of 
growth.  At  times  there  arc  no  nodules;  the  pleural  surface  is  merely 
uneven  and  apparently  diffusely  involved.  The  tissue  is  hard  and 
tough  on  section.  Ulceration  is  not  found.  Adhesions  are  common. 
A  variable  amount  of  bloody,  less  commonly  serous,  rarely  purulent 
fluid  is  usually  present. 

On  microscopic  examination  the  thickened  pleura  is  found  to  be 
made  up  of  aggregations  of  cells,  of  an  epithelial  character,  and  con- 
nective tissue,  each  in  varying  proportions  in  different  parts  of  the 
sections.  In  places  corresponding  to  the  nodules  seen  on  gross  inspec- 
tion, the  tumor  cells  are  closely  packed  together,  forming  small  groups, 
separated  by  a  thin  stroma.  In  the  intervening  tissue  and  in  places 
where  the  growth  is  more  diffuse  the  stroma  may  predominate  with 
scattered  round,  oval,  or  elongated  groups  of  epithelial-like  cells  in 
alveolar  arrangement,  in  few  or  many  of  which  a  lumen  may  be  seen 
and  a  resemblance  to  tubule  formation.  Small  areas  of  necrosis  are 
occasionally  present.  The  connective  tissue  is  usually  poor  in  cells, 
but  in  places  is  infiltrated  with  varying  numbers  of  small  round  cells. 
The  epithelium  of  the  free  surface  of  the  pleura  is  usually  absent  over 
the  whole  or  greater  part  of  the  sections,  and  in  most  of  the  cases  has 
not  apparently  taken  part  in  the  new  growth.  The  bloodvessels, 
which  may  be  increased  in  size  and  number,  have  likewise  been  unin- 
vaded  in  most  of  the  cases.  The  lymph  vessels  and  spaces  appear  to 
be  the  principal  site  of  the  new  growth,  and  to  many  observers  their 
endothelium  its  points  of  origin.  An  apparent  transition  from  the  flat 
cells  lining  the  lymph  channels  to  the  larger  polymorphous  epithelial- 
like  tumor  cells,  with  vesiculated  nuclei  and  variable  amount  of  gran- 
ular protoplasm,  has  frequently  been  noted.  In  some  of  the  reported 
cases  and  in  places  in  sections  I  have  studied,  the  groups  of  tumor 
cells  partly  or  wholly  fill  lymph  channels,  the  endothelium  of  which 
appears  quite  normal.  Rarely,  the  surface  epithelium  of  the  pleura 
appears  to  have  participated  in  the  proliferation.  In  Benda's  case1 
the  pleural  surface  was  beset  with  small  nodules;  on  microscopic 
examination  it  presented  a  villous-like  appearance,  and  he  observed 
an  apparent  transition  from  surface  epithelium  to  the  tumor  cells. 
It  seems,  however,  quite  impossible  to  judge  whether  the  tumor  cells 
arise  from  proliferation  of  cells  already  existing  in  the  part  or  are 
invading  the  tissue  through  the  lymph  channels. 

Metastases  have  been  observed  in  the  supraclavicular  glands  (Frankel 
and  Bonheim),  the  axillary  glands  (Neelsen),  and  the  thoracic  muscles 
(Xeelsen,  Perls,  Pirckner,  Glockner,  and  Schulz),  spontaneously  or 
along  the  needle  track,  after  withdrawal  of  pleural  fluid  (Podack  and 

1  Deut.  med.-Woch.,  1897,  No.  21,  p.  324. 


TUMORS  OF  THE  PLEURA  553 

Scagliosi).  The  disease  has  usually  invaded  other  organs  when  death 
occurs.  The  most  frequent  site  of  secondary  deposits  is  in  the  lungs. 
The  bronchial,  tracheal,  mediastinal,  retroperitoneal,  and  mesenteric 
glands,  the  viscera,  other  serous  membranes,  etc.,  may  be  the  site  of 
metastases.  In  six  of  the  reported  cases  (Wagner,  Bohme,  Teixeira 
de  Mattos,  Benda,  Scagliosi,  and  Bonheim)  no  metastases  were  found. 
In  the  presence  of  carcinoma  elsewhere  than  in  the  pleura  and  espe- 
cially with  the  disease  in  the  lungs,  it  is  never  certain  that  the  pleural 
disease  is  primary. 

Symptoms. — The  disease  usually  begins  like  an  ordinary  pleuritis, 
and  in  its  course  closely  resembles  pleural  tuberculosis.  Pain  is  usually 
a  prominent  symptom  and  is  often  increased  by  a  long  breath  and 
cough.  Dyspnea  and  cough  are  not  usually  striking  features  at  first, 
but  may  be  present  without  invasion  of  the  lung.  In  the  presence 
of  pleural  fluid,  dyspnea  may  be  extreme  and  orthopnea  may  be 
present.  If  the  lung  is  involved  the  sputum  may  contain  blood.  Fever 
is  usually  absent.    Loss  of  flesh  and  strength  is  usually  progressive. 

An  accumulation  of  pleural  fluid  is  almost  constant  and  the  physical 
signs  are  such  as  are  commonly  found  with  pleural  fluid  from  other 
causes,  although  certain  additional  features  may  permit  a  probable 
diagnosis.  The  progressive  loss  of  flesh  and  strength  will  naturully 
suggest  a  severe  disturbance.  The  absence  of  signs  pointing  to  disease 
in  the  apices  of  the  lungs,  the  failure  to  find  tubercle  bacilli  in  the 
sputum,  and  the  afebrile  course  may  argue  against  tuberculosis;  a 
negative  tuberculin  injection  may  positively  exclude  it.  The  presence 
of  metastases  in  accessible  regions  may  be  an  important  sign.  Inocula- 
tion metastases  in  the  course  of  the  needle  track  are  especially  impor- 
tant and  suggestive  and  should  always  be  sought  in  suspected  cases. 
They  are  usually  small,  flat,  hard,  slightly  movable,  and  painless. 
Invasion  of  the  needle  track  with  tuberculous  material  from  the  pleura 
may  likewise  occasionally  give  rise  to  similar  nodules  and  thus  their 
excision  and  microscopic  examination  may  be  necessary  to  establish 
the  diagnosis. 

On  examination  of  the  thorax,  diminished  expansion  of  the  affected 
side  may  be  a  striking  feature.  During  the  early  part  of  the  disease 
the  side  may  be  more  prominent,  to  appear  somewhat  smaller  later, 
with  relatively  narrow  and  less  depressed  interspaces.  With  effusion, 
the  heart  may  be  displaced,  returning  at  first  to  its  former  position 
after  the  withdrawal  of  the  fluid.  As  the  new  growth  gradually  invades 
a  larger  territory  and  as  the  pleura  becomes  thicker  and  less  elastic, 
with  the  formation  of  adhesions,  the  heart  often  fails  to  return  to  a 
position  which  it  might  be  expected  to  assume  after  the  removal  of  such 
an  amount  of  fluid.  For  similar  reasons,  the  thoracic  distress  and 
sense  of  pressure  are  afforded  progressively  less  relief  from  the  evacua- 
tion of  the  fluid,  which  reaccumulates  more  rapidly.  The  operator 
may  also  be  able  to  appreciate  the  much  thickened  and  tough  pleura 
by   the  resistance  offered  in  the  introduction  of  the  trocar.     The 


554  DISEASES  OF   THE  PLEURA 

physical  signs  may  show  little  if  any  change  after  the  removal  of 
even  large  amounts  of  fluid. 

Examination  of  the  pleural  fluid  may  afford  important  data  for 
diagnosis.  It  is  often  serous  at  first,  becoming  blood-tinged  or  even 
strongly  hemorrhagic  after  the  first  or  the  first  few  tappings.  This  is 
due  to  the  inelastic  character  of  the  pleural  walls,  and  probably,  too, 
as  examination  of  seetions  shows,  to  the  not  infrequent  presence  of 
bloodvessels  near  the  free  surface  of  the  pleura,  from  which  under  the 
influence  of  increased  negative  pleural  pressure  following  removal  of 
the  fluid,  blood  is  readily  extravasated.  With  the  progress  of  the 
disease  and  the  frequent  repetition  of  tapping,  the  fluid  may  resemble 
pure  venous  blood  or  have  a  chocolate  color.  That  its  bloody  char- 
acter is  associated  with  the  use  of  the  trocar  is  suggested  by  the  more 
frequent  bloody  character  of  the  fluid  in  cases  in  which  fluid  has  been 
withdrawn  and  the  occurrence  of  serous  fluid  in  cases  which  have 
been  allowed  to  run  their  course  without  such  interference.  The 
specific  gravity,  when  taken,  has  usually  been  1018  or  under.  Micro- 
scopic examination  of  the  sediment  may  assist  in  a  decision  between 
malignant  disease  and  tuberculosis.  In  carcinoma  of  the  pleura  there 
is  usually  a  much  larger  proportion  of  endothelial  cells,  with  a  relatively 
small  proportion  of  lymphocytes,  the  cytologic  formula  thus  conform- 
ing to  that  in  fluids  due  to  stasis.  There  is  no  reason  to  believe  that 
the  large  cells,  with  vesiculated  nuclei  and  vacuolated  protoplasm, 
not  infrequently  found  in  plaques,  are  other  than  desquamated  cells 
from  the  free  surface  of  the  pleura.  In  my  opinion  there  is  no  strik- 
ing or  constant  difference  between  these  large  cells  in  cases  of  stasis 
and  in  malignant  new  growths  of  the  pleura.  The  glycogen  reaction 
is  found  in  cells  from  pleural  fluid  of  other  than  malignant  origin. 
The  presence  of  many  cells  showing  typical  or  atypical  mitoses  has 
been  thought  diagnostic  of  malignant  disease. 

It  may  rarely  happen  that  the  microscopic  examination  of  a  small 
piece  of  tissue  removed  with  the  needle  may  establish  the  diagnosis. 

Prognosis. — The  disease  usually  terminates  fatally  within  six  months 
of  the  discovery  of  the  pleural  invasion.  A  period  of  eighteen  to 
twenty  months  may  elapse  between  the  beginning  of  symptoms  and 
the  fatal  termination. 

Treatment. — This  is  largely  symptomatic.  Removal  of  the  pleural 
fluid  usually  affords  only  temporary  relief.  At  times  it  has  been 
followed  by  marked  improvement,  especially  in  the  early  stages  of 
the  disease.  As  the  disease  progresses,  distressing  pressure  symptoms 
usually  necessitate  more  frequent  withdrawal,  and  not  infrequently 
with  less  and  less  relief.  At  times,  with  much  thickening  of  the  visceral 
pleura,  removal  of  fluid  may  only  aggravate  the  symptoms,  from 
increased  tension  on  a  retracted  and  adherent  lung.  Morphin  in 
sufficient  doses  is  of  value  and  may  prolong  the  necessary  intervals 
between  the  tappings.  The  repeated  removal  at  short  intervals  of 
a  very  bloody  fluid  may  hasten  the  fatal  termination,  but  in  considera- 


TUMORS  OF  THE  PLEURA  555 

tion  of  the  relief  of  distressing  symptoms  its  evacuation  seems  justi- 
fiable if  other  means  fail.  It  is  better  to  withdraw  small  amounts  fre- 
quently than  to  empty  the  cavity  at  each  tapping.  Free  drainage 
of  the  pleural  cavity  by  resection  of  a  rib  has  been  followed  by  a 
change  in  the  character  of  the  pleural  fluid  from  bloody  to  serous. 

Sarcoma. — Primary  sarcoma  is  even  less  common  than  primary 
carcinoma  in  the  pleura.  Although  in  some  of  the  reported  eases 
a  distinction  has  not  been  made  between  the  two  groups,  this  is  justi- 
fied from  the  general  character  and  histologic  appearance.  Twelve 
cases  will  be  found  referred  to  and  summarized  by  Bloch.1  Mehrdorf2 
has  reviewed  the  literature.  Bernard3  found  24  reported  cases.  Only 
one  case4  has  come  under  my  observation.  Of  14  cases  which  I  have 
analyzed  9  occurred  in  males.  The  ages  varied  from  seven  to  seventy- 
six.  Of  the  remaining  patients,  2  were  from  ten  to  twenty,  4  from 
twenty  to  thirty,  2  from  thirty  to  forty,  1  from  forty  to  fifty,  2  from 
fifty  to  sixty,  and  1  from  sixty  to  seventy.  The  two  sides  are  about 
equally  affected.  In  their  clinical  course  they  resemble  primary 
carcinoma  of  the  pleura.  A  collection  of  pleural  fluid  practically 
always  accompanies  the  new  growth,  and  this  is  usually  bloody,  rarely 
serous.  Its  hemorrhagic  character  may  first  appear  only  after  tap- 
ping. The  presence  of  spindle  cells  in  the  sediment  may  suggest 
spindle-celled  sarcoma  of  the  pleura,  as  in  Warthin's  case. 

In  gross  character  at  autopsy,  primary  sarcoma  of  the  pleura  usually 
presents  a  different  appearance  from  primary  carcinoma.  In  rare 
instances,  however,  as  in  primary  carcinoma,  the  pleura  may  be 
diffusely  and  homogeneously  invaded.  Rarely,  there  are  innumer- 
able small  nodules,  but  the  new  growth  is  commonly  single,  hard,  or 
soft,  its  surface  smooth  or  lobulated,  in  color  white,  gray,  or  reddish, 
of  variable  and  usually  considerable  size,  even  at  times  reaching  that 
of  a  man's  head.  The  pleura  may  cover  the  growth  which  appears 
to  arise  in  the  subserous  tissue.  In  other  cases  no  traces  of  pleura  can 
be  found,  and  the  tumor  itself  forms  the  lining  of  the  pleural  sac,  yet 
ulceration  is  uncommon.  Invasion  of  neighboring  organs  by  exten- 
sion or  metastases  in  the  lungs,  the  neighboring  glands,  ribs,  verte- 
brae, liver,  spleen,  or  superficial  parts  of  the  body  has  occurred.  In 
3  cases  no  metastases  were  found.  From  their  microscopic  appear- 
ance the  tumors  have  been  classed  as  simple  sarcoma,  round,  spindle- 
celled,  fibrosarcoma,  and  myxosarcoma.  Garre5  successfully  removed 
a  spindle  and  round-celled  sarcoma  weighing  1250  grams  from  the 
left  pleura. 

1  Les  Neoplasms  malins  primitifs  de  la  plevre,  Paris,  Vigot  Freres,  1905. 

2  Virchow's  Arch.,  1908,  Bd.  exciii. 

3  Ibid.,  1913,  ccxi,  156. 

4  An  unpublished  case  of  H.  A.  Christians. 

6Verhandl.  d.  deut.  Gesellsch.  f.  Chir.,  1909,  2  Th„  xxxviii,  121. 


556  DISEASES  OF   THE  PLEURA 

SECONDARY    MALIGNANT    TUMORS. 

Malignant  disease  of  the  pleura  is  more  commonly  secondary  than 
primary.  The  tissue  may  be  invaded  by  metastases  from  a  primary 
malignant  tumor  in  any  part  of  the  body,  but  pleural  invasion  is  more 
common  in  malignant  disease  of  the  lung,  mediastinum,  thoracic- 
wall,  or  stomach.  Metastatic  new  growths  of  the  pleura  do  not  usually 
produce  a  diffuse  infiltration  of  the  tissue.  There  are  commonly 
several  isolated  nodules  or  masses  and  more  rarely  the  pleura  presents 
a  generally  nodular  appearance.  Pleural  fluid  may  or  may  not  be 
present,  and  this  may  be  serous,  but  is  more  commonly  bloody.  In 
cases  of  pleural  carcinoma  secondary  to  the  disease  in  the  breast, 
the  clinical  picture,  course,  and  termination  may  resemble  primary 
carcinoma  of  the  pleura. 

Of  178  cases  coming  to  autopsy  at  the  Massachusetts  General 
Hospital  with  carcinoma  in  various  regions,  10  showed  •  secondary 
deposits  in  the  pleura.  Of  10  cases  with  carcinoma  of  the  breast,  the 
pleura  was  invaded  in  4.  Of  58  cases  in  which  the  disease  was  primary 
in  the  stomach,  only  3  showed  pleural  metastases.  In  this  series, 
carcinoma  of  the  pleura  was  also  secondary  to  the  disease  in  the 
thymus  and  ovary.  Of  42  cases  of  sarcoma,  primary  in  various 
regions,  the  pleura  was  secondarily  invaded  in  9. 


CHAPTER  XXXV. 
ECHINOCOCCUS  DISEASE  OF  THE  PLEURA. 

Etiology. — Following  the  ingestion  of  the  egg  of  Taenia  echinococcus, 
the  embryo,  liberated  from  its  shell  in  the  stomach,  may  migrate  to 
the  pleura.  The  course  pursued  in  reaching  the  pleura  is  uncertain, 
but  the  more  frequent  infection  of  the  right  pleura  suggests  a  migra- 
tion by  way  of  the  portal  blood  stream  or  biliary  channels  to  the  liver, 
thence  through  the  diaphragm  to  the  pleura.  Infection  may  also  be 
direct  or  by  way  of  the  lymph  channels  or  the  systemic  circulation. 

Special  Pathology. — It  is  convenient  to  divide  cases  into  those  in 
which  the  disease  apparently  arises  within  the  pleural  sac  or  the  pleural 
tissues:  (A)  Pleural  Echinococcus:  The  difficulty  of  distinguishing 
cysts  of  the  pleura  from  those  developing  in  its  neighborhood  and 
the  frequency  with  which  the  latter  lead  to  disturbances  in  the  pleura, 
justifies  a  further  division  of  cases  into  (B)  Parapleural  echinococcus, 
in  which  the  primary  infection  has  taken  place  in  a  neighboring  organ, 
but  in  its  growth  the  cyst  encroaches  upon  and  develops  at  the  expense 
of  the  pleural  space. 

(1)  Pleural  Echinococcus. — (a)  Primary. — The  exact  site  of  the  pri- 
mary infection  is  uncertain,  as  cases  come  under  observation  with  the 
cysts  already  developed  to  a  considerable  size.  The  number  of  cases  in 
which  the  disease  is  primary  in  the  pleura  is  small.  In  the  combined 
statistics  of  Neisser  and  Madelung,  among  1179  cases,  echinococcus 
was  primary  in  the  pleura  in  only  18  (1.5  per  cent.).  This  report  is 
based  on  43  cases.1  The  right  pleura  was  involved  in  25,  the  left  in 
10;  in  8  the  site  was  not  given. 

The  cyst  is  usually  situated  at  the  lower,  but  may  be  confined  to 
the  upper  part  of  the  pleural  cavity.  The  local  reaction  leads  to  the 
formation  of  a  connective- tissue  envelope,  which  is  usually  very  thin, 

1  Neisser,  Die  Echinococcus  Krankheit,  Hirschwald,  Berlin,  1877,  17  cases;  Made- 
lung,  Beitrage  zur  Lehre  von  der  Echinococcen-Krankheit,  Stuttgart,  1885,  2  cases; 
Maydl,  Ueber  Echinokokkus  der  Pleura,  Wien,  1891  (cases  8,  9,  11),  3  cases;  Theophil 
Rosenthal,  Diss.,  1881  (quoted  from  Winzerling),  5  peripleural  cases;  Winzerling, 
Ein  Beitrag  zur  Casuistik  des  primaren  Pleuraechinococcus,  Inaug.  Diss.,  Jena,  1892, 
3  cases;  Mosler  and  Peiper,  Nothnagel's  Spec.  Path.  u.  Ther.,  Bd.  vi,  1  case  mentioned; 
Ascoli,  Rendiconto  della  Societa  Lancisiana  (quoted  from  Orlandi),  4  cases;  Vannini, 
Bulletino  delle  scienze  Mediche  di  Bologna,  1896,  p.  240,  1  case;  Pasca,  Rendiconto 
Societa  Lancisiana  degli  Ospedali,  Roma,  27  giugno,  1896,  1  case;  Orlandi,  Gazetta 
medica  di  Torino,  1898,  p.  49,  1  case;  von  Bokay,  "Festschrift"  in  honor  of  Abraham 
Jacobi,  New  York,  1900,  1  case;  Cary  and  Lyon,  Trans.  Assoc.  Amer.  Phys.,  1900, 
vol.  xv,  1  case;  Blechmann,  Ueber  primaren  Echinococcus  der  Pleura,  Inaug.  Diss., 
Kiel,  1901,  1  case;  Hauser,  Primarer  Echinococcus  multilocularis  der  Pleura  und  der 
Lunge  mit  entwicklung  multipler  Metastasen  im  Gehirn,  Erlangen  u.  Leipzig,  1901, 
1  case;  Ransom  and  Willis,  British  Med.  Jour.,  1903,  i,  302,  1  case. 


558  DISEASES  OF  THE  PLEURA 

hut  may  be  thick.  Pleuritis  is  uncommon.  Enlargement  of  the  sac 
gradually  compresses  or  displaces  neighboring  organs.  Perforation 
may  occur  into  the  lungs  with  evacuation  through  the  bronchi;  or 
erosion  of  the  ribs  and  intercostal  spaces  may  lead  to  rupture  through 
the  chest  wall.  Both  are  rare.  The  cyst  may  become  infected,  and 
presents  the  appearance  of  an  encysted  empyema.  The  most  common 
type  is  a  single  cyst  or  one  sac  containing  daughter  cysts  (endogenous 
echinococcus).  Rarely  more  than  one  cyst  is  found.  A  pleural  cyst 
with  multiple  external  budding  (exogenous  echinococcus)  is  described 
by  Cary  and  Lyon,  and  an  alveolar  echinococcus  (Echinococcus  multi- 
loeularis),  apparently  primary  in  the  pleura  and  with  coincident  or 
metastatic  multilocular  cysts  in  the  lung,  the  diaphragm,  psoas 
muscle,  and  brain  is  reported  by  Hauser.  The  localization  of  cysts  in 
the  peripleural  tissue,  between  the  costal  pleura  and  the  thoracic  wall, 
is  difficult  to  determine.  Their  separate  consideration  is  hardly  justi- 
fiable, as  they  probably  represent  cysts  arising  in  the  pleural  or  sub- 
pleural  tissue,  the  development  of  which  toward  the  lungs  is  prevented 
by  dense  adhesions. 

(b)  Secondary. — 1.  By  Metastasis. — It  is  still  an  open  question 
whether  an  echinococcus  cyst,  primary  in  the  pleura,  can  give  rise  to 
metastases  in  other  and  remote  parts  of  the  body.  It  is  likewise 
uncertain  whether  unruptured  cysts  in  parts  distant  from  the  pleura 
can  lead  to  secondary  pleural  invasion.  The  weight  of  opinion  is 
rather  that  multiple  and  isolated  cysts  are  due  to  infection  with  more 
than  one  Taenia  echinococcus  embryo  at  the  same  or  at  different 
times. 

2.  By  Extension. — Auto-infection  through  rupture  of  the  mother 
cyst,  the  evacuation  of  daughter  cysts  into  neighboring  tissues  and 
their  further  development  is  established  for  abdominal  echinococcus. 
A  similar  secondary  infection  of  the  pleura  from  the  rupture  of  pul- 
monary or  hepatic  cysts  may  take  place,  but  pleural  infection  with 
bacteria  usually  precedes  or  so  quickly  follows  the  rupture  that  unless 
operation  is  undertaken,  death  almost  always  occurs  within  a  variable 
and  usually  short  period. 

(2)  Parapleural  Echinococcus. — (a)  Intact  Cysts. — In  this  class  may  be 
included  cases  in  which  the  disease  develops  in  neighboring  organs, 
but  encroaches  upon  and  grows  at  the  expense  of  the  pleural  space.  The 
cases  comprise  for  the  most  part  those  in  which  cysts  are  present  in 
the  peripheral  parts  of  the  lung,  the  upper  part  of  the  liver,  or  the 
region  between  the  liver  and  the  diaphragm;  and  more  rarely  echino- 
coccus disease  of  the  mediastinum,  spleen,  or  kidney.  The  clinical 
picture  may  be  quite  indistinguishable  from  primary  pleural  echino- 
coccus. Subdiaphragmatic  and  especially  hepatic  cysts  are  most 
common  and  the  diaphragm  may  be  elevated  to  the  second  rib  and 
even  to  the  clavicle.  In  both  the  subdiaphragmatic  and  pulmonary 
forms  of  the  disease  the  heart  may  be  displaced  laterally,  the  liver 
dislocated  downward.     The  condition  of  the  pleura  in  the  presence 


ECHINOCOCCUS  DISEASE  OF  THE  PLEURA  559 

of  an  echinococcus  cyst  in  its  neighborhood  is  variable  and  depends 
to  some  extent  on  the  presence  or  absence  of  suppuration  in  the  cyst. 
The  visceral  and  parietal  layers  may  be  free,  serous  or  purulent  pleural 
fluid  may  be  present,  but  partial  or  complete  adherence  of  its  layers 
is  more  common  and  more  favorable,  as  rupture  of  the  cyst  may  then 
fail  to  infect  the  pleura. 

(b)  Perforated  Cysts. — According  to  Neisser's  statistics,  echinococcus 
disease  of  the  liver  breaks  through  into  the  respiratory  apparatus 
in  about  11  per  cent,  of  the  cases.  Disturbances  of  the  pleura  from 
parapleural  echinococcus  are  more  common  than  from  the  primary 
disease.  Depending  on  the  previous  condition  of  the  pleura  and  the 
character  of  the  cyst  contents,  rupture  is  followed  by  free  or  encysted, 
cystic,  serous,  or  purulent  fluid.  Suppuration  is  practically  a  con- 
stant feature.  The  perforation  of  an  adherent  pleura  with  invasion 
of  the  lung  or  bronchi  is  most  common.  Of  30  cases  in  Davaine's 
series  only  9  ruptured  into  the  pleura,  21  into  the  lung  or  bronchi. 
In  Neisser's  60  cases  the  pleura  was  invaded  in  16,  the  lung  in  12,  and 
the  bronchi  in  32.  Hepatopleural  or  hepatobronchial  fistulse  may 
result,  and  bile  may  be  found  in  the  pleural  cavity  or  even  be  expec- 
torated. An  echinococcus  cyst  of  the  lung  may  likewise  lead  to  free 
or  encysted  and  usually  purulent  pleural  fluid,  following  rupture.  If 
the  pleurae  are  adherent  the  pulmonary  cyst  may  evacuate  externally. 
Rupture  into  the  bronchi  is,  however,  more  common. 

Symptoms. — In  rare  instances  there  may  be  no  symptoms.  In  cases 
in  which  the  disease  is  primary  in  the  pleura  the  symptoms  are  usually 
those  of  a  slowly  growing  intrathoracic  tumor.  Cough  may  be  absent 
or  present,  with  .scanty  mucoid  sputum  from  an  accompanying  bron- 
chitis. Dyspnea  is  usually  present  and  is  progressive.  There  may 
be  pain  with  respiration,  but  this  is  not  a  striking  feature  unless  pleu- 
ritis  is  present.  Fever  is  usually  absent.  Emaciation  is  not  common 
in  uncomplicated  cases.  The  perforation  of  pleural  cysts  into  the 
lung  is  rare.  Septic  pneumonia  and  even  abscess  and  gangrene  may 
follow.  If  there  is  free  communication  with  the  bronchi,  clear  cystic 
fluid  may  be  expectorated.  In  this  or  in  evacuated  pus,  hooklets  or 
bits  of  cyst  membrane  may  be  discovered.  Rupture  may  occur  through 
the  chest  wall,  following  atrophy  of  the  intercostal  muscles  and  erosion 
of  the  ribs.  Spontaneous  rupture  is  likely  to  occur  if  the  cyst  has  sup- 
purated. The  perforation  of  parapleural  echinococcus  into  the  pleura 
is  less  common  than  into  the  lung.  Rupture  may  take  place  without 
symptoms;  in  other  cases  the  patient  may  be  conscious  of  the  rup- 
ture, which  is  followed  by  pain  of  a  severe  character,  and  if  suppura- 
tion is  present,  as  is  commonly  the  case,  there  is  chill  and  fever.  Rup- 
ture may  be  spontaneous,  or  may  be  induced  by  exertion  or  trauma. 
If  sinuses  connect  with  the  liver,  biliary  coloring  matter  may  be 
expectorated.  Hepatic  echinococcus  cysts  may  perforate  the  pleura 
and  be  evacuated  through  the  lung  without  characteristic  elements 
in  the  sputum,  in  case  the  bile  passages  fail  to  connect  with  the  cyst. 


560  DISEASES   OF    THE    1'LECh'A 

Urticaria  may  follow  the  rupture  of  pleural  echinococcus  into  the 
pulmonary  or  other  tissues  or  of  parapleural  cysts  into  the  pleura. 
Severe  symptoms  of  intoxication,  even  delirium,  collapse,  and  death 

may  likewise  follow  the  rupture. 

The  duration'  of  pleural  echinococcus  is  difficult  to  determine.  To 
judge  from  its  growth  in  accessible  regions  it  may  take  from  six  months 
to  a  year  for  it  to  reach  the  size  of  the  fist.  Symptoms  may  arise  only 
after  it  has  attained  a  large  size. 

On  examination  the  signs  are  usually  those  of  encysted  pleural 
fluid.  There  is  diminished  expansion  of  the  affected  side,  which  is 
likely  to  be  prominent,  with  obliteration  of  the  normal  intercostal 
depressions.  The  side  may  be  dull  or  flat  on  percussion  and  in  some 
eases  it  is  possible  to  note  an  irregular  or  evenly  curved  arching  of 
the  upper  border  of  dulness,  the  convexity  of  which  is  directed  upward. 
The  tactile  fremitus  and  breathing  are  diminished  or  absent;  the 
latter  may  have  a  bronchial  quality.  The  voice  sounds  are  dimin- 
ished and  pegophony  may  be  present.  The  signs  are  likely  to  be  atypi- 
cal. Between  the  involved  area  and  the  lung  there  may  be  an  abrupt 
transition  on  auscultation  to  normal  vesicular  breathing.  In  the 
presence  of  a  large  cyst  fluctuation  may  possibly  be  made  out,  but 
the  hydatid  fremitus  or  quivering  of  jelly  sensation  has  not  been 
observed.  The  liver  or  spleen  may  be  displaced  downward,  the  heart 
to  the  right  or  left.  The  presence  of  echinococcus  cysts  elsewhere 
in  the  body  may  suggest  a  similar  affection  of  the  pleura. 

Blood. — The  presence  of  eosinophilia  in  the  circulating  blood  may  be 
confirmatory.  Cabot  collected  30  cases  of  hydatid  of  the  liver,  only 
2  of  which  were  negative.  Of  20  cases  in  Welsh  and  Barling's  series, 
all  but  5  exceeded  the  average  in  health. 

Diagnosis. — Infection  with  echinococcus  is  rare  in  North  America 
and  Great  Britain,  and  cases  wdiich  occur  are  for  the  most  part  in 
foreigners.  A  previous  residence  where  the  disease  is  prevalent,  and 
contact  with  dogs  used  for  herding  sheep,  may  be  suggestive.  Posi- 
tive data  for  diagnosis  are  furnished  by  the  discovery  of  scolices, 
hooklets,  or  cyst  membrane.  If  perforation  has  occurred  into  the 
lung,  such  material  may  be  present  in  the  expectoration.  An  urti- 
carial rash  following  thoracentesis  is  very  suggestive.  The  examina- 
tion of  the  fluid  obtained  by  pleural  puncture  may  furnish  suggestive 
chemical  features.  It  is  usually  clear,  transparent,  and  varies  from 
1009  to  1012  in  specific  gravity.  Sodium  chloride  is  present.  Albu- 
min is  usually  absent  or  present  only  in  traces.  Traces  of  inosit, 
succinic  acid,  and  grape-sugar  may  be  found,  and  although  suggestive 
are  not  distinctive  of  the  disease.  In  some  cases  the  specific  gravty 
is  high  and  the  amount  of  albumin  considerable.  If  degeneration  has 
taken  place,  cholesterin  crystals  may  be  found.  If  infection  has 
occurred,  it  may  mask  the  appearance  of  the  fluid.  Specific  anti- 
bodies in  the  blood  of  patients  with  echinococcus  disease  may  be 
demonstrated  by  the  complement  fixation  test.     The  antigen  may 


ECHINOCOCCUS  DISEASE  OF  THE  PLEURA  5til 

be  made  from  the  cyst  fluid  or  an  alcoholic  extract  of  the  cyst  mem- 
brane.   Kreuter1  has  reviewed  the  literature. 

A  resort  to  thoracentesis  for  the  diagnosis  of  pleural  or  pulmonary 
echinococcus  is  attended  by  considerable  danger,  for  perforation  of 
the  enveloping  connective-tissue  sac  and  the  cyst  membrane  may 
result  in  the  evacuation  of  the  cyst  fluid  into  the  pleura  or  the  lung, 
if  erosion  of  its  substance  has  already  occurred.  As  the  perforated 
cyst  membrane  is  subjected  to  changes  of  intrathoracic  pressure  with 
respiration  or  cough,  the  contained  fluid  may  find  its  way  between 
the  connective-tissue  envelope  and  cyst  membrane  to  the  bronchi. 
Urticaria,  symptoms  of  severe  intoxication,  with  gastro-intestinal 
disturbances,  faintness,  collapse,  delirium,  and  even  coma,  and  death 
may  result.  Pulmonary  or  pleural  suppuration  or  suffocation  from 
mechanical  obstruction  by  fluid  or  cysts  may  occur.  Maydl  reports 
11  cases  of  pleural  or  pulmonary  echinococcus  in  which  a  fatal  result 
followed  thoracentesis.  When  we  consider  the  infrequency  of  the 
disease,  this  is  a  warning  which  cannot  be  safely  disregarded.  If  the 
diagnosis  can  be  made  without  puncture  it  is  better  to  resort  to  opera- 
tion without  previous  exploration.  If  thoracentesis  is  done,  a  small 
trocar  (not  a  needle)  is  less  dangerous,  and  if  the  case  proves  to  be 
echinococcus,  operation  should  be  at  once  undertaken. 

The  pleural,  pulmonary,  or  subdiaphragmatic  site  may  be  difficult 
to  determine  and  the  different  forms  may  coexist.  In  Patella's  case'2 
the  diagnosis  before  operation  was  pleural,  after  operation  hepatic, 
and  at  autopsy  pulmonary  echinococcus.  Centrally  placed  pulmo- 
nary cysts  may  be  without  signs.  The  cyst  is  usually  single  and 
in  the  lower  lobes,  more  commonly  the  right.  With  a  cyst  in  the 
•peripheral  parts  of  the  lung  the  signs  are  usually  the  same  as  in 
pleural  echinococcus.  Pain  is  less  often  present,  dyspnea  may  be 
more  paroxysmal,  cough  is  likely  to  be  more  troublesome,  and  the 
sputum  may  be  bloody.  '  Rupture  into  the  bronchi  is  more  common 
in  pulmonary  than  in  pleural  cysts.  The  differentiation  is  often 
impossible  during  life,  and  even  at  autopsy  it  may  be  uncertain  whether 
the  growth  started  in  the  lung  or  the  pleura.  Subdiaphragmatic 
cysts  which  may  be  confused  with  the  pleural  or  pulmonary  form 
usually  involve  the  liver  at  its  upper  part  or  the  space  between  liver 
and  diaphragm.  In  either  case  the  diaphragm  is  elevated,  the  lung 
compressed,  the  heart  displaced  to  the  right  or  left,  and  the  liver 
depressed.  The  clinical  picture  may  then  resemble  pleural  echino- 
coccus, but  the  depression  of  the  liver  and  the  lateral  dislocation  of 
the  heart  are  less  marked.  Cough  may  be  absent  and  dyspnea  less 
troublesome.  The  greater  vertical  excursion  of  the  lower  pulmonary 
margin  and  the  presence  of  the  diaphragm  phenomenon,  with  sub- 
diaphragmatic   cysts,    may    be    important    differential    signs.     The 

1  Beitr.  z.  klin.  Chir.,  vol.  lxxvi. 

2  Quoted  from  Maydl,  loc.  cit.,  p.  71. 
36 


562  DISEASES  OF   THE   PLEURA 

distinction  between  an  intrathoracic  and  intra-abdominal  cyst  is 
important  for  surgical  interference. 

Echinococcus  cysts  may  be  confused  with  benign  or  malignant 
new  growths  of  the  pleura  and  encysted  or  free  pleural  fluid. 
Benign  tumors  are  so  rare  as  to  need  no  special  consideration. 
Aside  from  the  history  of  opportunities  for  infection  in  echino- 
coccus and  the  presence  of  cysts  elsewhere,  the  differentiation  can 
hardly  be  made.  Secondary  pleural  carcinoma  or  sarcoma  can 
usually  be  excluded  by  the  presence  of  a  primary  focus  elsewhere. 
In  primary  malignant  disease  the  course  is  more  progressively  down- 
ward, with  loss  of  flesh  and  strength.  Superficial  metastases  may 
be  found.  Pain  is  a  more  prominent  symptom.  Owing  to  the  diffuse 
character  of  the  process,  the  whole  or  a  greater  part  of  one  side  of  the 
chest  may  be  dull.  The  percussion  note  is  more  board-like,  and  if 
free  fluid  is  present  its  upper  border  may  show  a  characteristic  curve. 
In  the  later  stages  of  malignant  disease  the  affected  side  is  more  often 
somewhat  contracted.  If  inflammatory  fluid  is  present  there  is  often 
the  history  of  an  acute  onset  with  pain  and  fever.  There  may  be 
evidence  of  pulmonary  or  other  disease  to  which  the  pleural  fluid  is 
secondary.  The  pain  is  likely  to  subside  as  the  fluid  accumulates. 
Such  processes  seldom  last  as  long  and  the  accumulated  fluid  does  not 
as  slowly  and  steadily  increase.  With  free  fluid  the  line  of  demarca- 
tion between  it  and  the  lung,  determined  by  auscultation  and  percus- 
sion, is  less  abrupt  than  in  echinococcus  disease,  the  upper  limit  of 
flatness  may  have  a  characteristic  curve,  and  changes  in  level  may 
be  made  out  on  changing  the  position  of  the  patient.  If  encysted 
fluid  is  purulent,  its  character  may  be  suggested  by  symptoms  of 
sepsis.  The  appearance,  chemical  character,  and  microscopic  exami- 
nation of  fluid  obtained  by  puncture  afford  valuable  data  for  dif- 
ferential diagnosis.  Urticaria  following  exploratory  puncture  should 
suggest  echinococcus  disease. 

Prognosis. — This  is  practically  hopeless  for  cases  of  echinococcus 
cysts  of  the  pleura  or  the  parapleural  tissue  rupturing  into  the  pleura, 
and  allowed  to  run  their  course  without  treatment.  Of  31  unoperated 
cases  in  Neisser's  "statistics,"  including  12  pleural,  7  pulmonary  with 
pleural  perforation,  and  12  hepatic  with  pleural  perforation,  all  died. 
The  prognosis  is  much  worse  for  pleural  than  pulmonary  echinococcus 
in  which  perforation  into  the  lung  may  be  followed  by  recovery.  The 
prospect  in  operated  cases  is  much  more  encouraging.  Of  13  operated 
cases  of  pleural  echinococcus  in  Maydl's  statistics,  4  (30  per  cent.) 
died. 

Treatment. — Evacuation  of  the  cyst  contents  with  the  trocar,  with 
or  without  the  injection  of  solutions  containing  iodine  or  other  sub- 
stance, has  been  followed  by  cure,  but  is  uncertain  and  too  dangerous 
to  recommend.  The  high  mortality  following  puncture  of  the  cyst 
has  been  mentioned.  A  radical  operation  only  can  be  considered. 
Costatectomy  is  better  than  simple  incision.     If  possible,  the  cyst 


ECHINOCOCCUS  DISEASE  OF  THE  PLEURA  563 

should  be  removed  without  rupture.  If  too  large  to  he  removed 
entire,  the  cyst  membrane  may  be  drawn  into  the  wound  of  operation 
and  aspirated.  It  may  then  be  shelled  out  from  its  capsule.  As  it  is 
often  difficult  to  be  certain  that  the  cyst  is  not  pulmonary  or  sub- 
diaphragmatic, the  pleura  should  be  carefully  approached.  If  sup- 
puration of  the  sac  has  taken  place,  the  abscess  should  be  opened  and 
drained  as  in  other  suppurative  pleural  affections.  Subdiaphragmatic 
cysts  projecting  into  the  thorax  are  best  approached  through  the 
pleura. 


CHAPTER  XXXVI. 
PNEUMOTHORAX. 

By  this  is  understood  the  presence  of  atmospheric  air  or  gas  in 
the  pleural  cavity.  There  is  frequently  also  a  liquid  exudate,  hence 
the  terms  hydropneumothorax  with  serous,  pyopneumothorax  with 
purulent,  and  hemopneumothorax  with  bloody  fluid. 

Historical  Note. — The  splashing  sound  produced  by  succussion  is 
mentioned  in  the  works  commonly  ascribed  to  Hippocrates  and  is 
frequently  spoken  of  as  "Hippocratic  succussion,"  but  the  condition 
in  which  it  was  noted  was  regarded  as  empyema,  the  distinction 
between  empyema  and  pneumothorax  not  being  clearly  appreciated. 
A  few  cases  were  described,  usually  of  the  traumatic  variety,  and  the 
mechanics  of  pneumothorax  were  fairly  understood  in  the  seven- 
teenth and  eighteenth  centuries,  but  the  thesis  of  Itard1  in  1803  is 
commonly  regarded  as  the  starting-point  of  the  modern  concep- 
tion of  the  disease.  Itard  named  the  condition  Pneumothorax  and 
recognized  its  relation  with  tuberculosis.  In  1819  Laennec  published 
the  most  important  contribution  up  to  that  time.  He  described  the 
causes,  symptoms,  and  physical  signs,  and  his  account  of  the  ausculta- 
tory phenomena  left  practically  nothing  to  be  added  by  those  who  have 
since  written  on  this  subject.  He  was  the  first  to  give  the  succussion 
splash  its  true  significance.  Emerson2  in  1903,  published  the  most 
elaborate  and  complete  treatise  on  the  disease  and  here  may  be  found 
an  abstract  of  many  important  articles.  Renewed  interest  has  recently 
been  aroused  in  artificial  pneumothorax  as  a  therapeutic  measure 
in  the  treatment  of  pulmonary  tuberculosis. 

Pathologic  Physiology. — An  appreciation  of  the  mechanical  factors 
is  essential  to  a  clear  understanding  of  pneumothorax. 

The  thorax  is  capable  of  rhythmic  changes  in  volume  during  inspira- 
tion and  expiration.  Inspirator}'  enlargement  is  accomplished  by 
the  contraction  of  muscles  applied  to  the  bony  framework  and  the 
descent  of  the  diaphragm.  Within  the  thoracic  cavity  the  lungs,  in 
communication  with  the  atmosphere  through  the  trachea,  hang  free 
and  unattached,  although  everywhere  in  close  apposition  to  its  walls. 
Since  the  pleural  sac  is  without  communication  with  atmospheric 
air  and  since  the  lungs  are  easily  distensible,  with  each  inspiratory 
enlargement  of  the  chest,  air  enters  the  trachea  and  inflates  the  lungs 

1  Dissertation  sur  le  pneumothorax  ou  les  congestions  gazeuses  qui  se  forment  dans 
la  poitrine,  Thesis,  Paris,  1803. 

2  Pneumothorax:  an  Historical,  Clinical,  and  Experimental  Study,  Johns  Hopkins 
Hosp.  Rep.,  1903,  vol.  xi. 


PNEUMOTHORAX  565 

much  as  one  fills  a  hand-bellows  with  air  by  separating  its  handles. 
The  lungs  are  not  only  easily  distensible  but  are  elastic  and 
are  stretched  in  both  phases  of  respiration  beyond  the  volume  they 
would  assume  if  the  pleural  cavity  were  open  and  in  free  communica- 
tion with  the  external  air.  Expiration  is  passive  and  due  to  the  elastic 
recoil  of  the  lungs  and  the  thoracic  and  abdominal  walls.  Owing 
to  the  constant  elastic  tension  of  the  lungs  there  is  in  the  potential 
pleural  space  a  negative  pressure  which  is  greater  during  inspiration 
than  in  expiration. 

Many  attempts  have  been  made  to  measure  this  normal  intrapleural 
tension  after  death  in  man  and  on  living  animals,  but  the  results  of 
such  observations  cannot  be  regarded  as  indicating  the  condition  in 
healthy  man.  The  most  trustworthy  figures  appear  to  be  those  of 
Aron,1  who  found  as  an  average  of  36  observations  the  maximum  read- 
ing for  quiet  inspiration  —5.09  and  the  minimum  for  expiration  —2.54 
mm.  Hg.  in  a  healthy  individual  willing  to  allow  a  manometer  to  be 
inserted  into  the  chest.  This  normal  tension  thus  demonstrated 
probably  varies  within  wide  limits  in  different  individuals.  In  the 
fetus  and  the  new-born  the  lungs  fill  the  chest  even  after  the  pleural 
space  is  perforated  and  there  is  no  pressure  difference,  which  first 
shows  itself  with  increasing  growth,  probably  because  the  thorax 
grows  more  rapidly  than  the  lungs.2  Pleural  adhesions  or  disease 
in  the  lung  and  mediastinum  are  also  likely  to  influence  the  pleural 
pressure  and  may  serve  to  explain  the  wide  differences  obtained  in 
the  measurement  of  intrapleural  tension  by  different  observers  and 
in  the  clinical  behavior  of  cases  of  pneumothorax. 

The  contention  of  West,3  that  between  the  pleural  surfaces  a  cohe- 
sive force  exists  sufficient  to  overcome  the  pulmonary  elasticity,  has 
been  the  subject  of  much  controversy.  Those  who  uphold  this  view 
maintain  that  the  so-called  normal  negative  intrapleural  tension  has 
no  real  existence,  but  is  latent  and  first  manifest  only  when  the  pleural 
surfaces  are  separated  in  an  effort  to  demonstrate  it.  To  Brauer4 
the  negative  pressure  determined  by  the  manometer  in  the  normal 
pleura  is  a  symptom  of  pneumothorax.  No  conclusive  evidence  for  or 
against  this  hypothesis  has  yet  been  offered. 

Owing  to  the  elastic  tension  of  the  lung  and  the  consequent  nega- 
tive pressure  in  the  potential  pleural  space,  the  admission  of  air  to  the 
pleural  cavity  is  followed  by  collapse  of  the  lung.  The  mechanical 
conditions  differ  somewhat,  depending  on  whether  the  communication 
of  the  pleural  space  with  the  outside  world  is  open,  valvular,  or  closed. 

Intrapleural  Pressure  in  Pneumothorax. — Observations  are  not 
numerous.  Among  them  Aron  reported  three  cases  illustrating  each 
form.    In  a  patient  operated  on  for  empyema  with  an  open  external 

1  Die  Mechanik  und  Therapie  des  Pneumothorax,  1902. 

2  Hermann,  Pfliiger's  Arch.,  1879,  xx,  365. 

3  British  Med.  Jour.,  August  20,  1887. 

4  See  Mosheim,  Beitrage  z.  Klinik  der  Tub.,  1905,  vol.  iii. 


5G6  DISEASES  OF   THE  PLEURA 

fistula  the  pressure  oscillated  about  the  zero  point,  with  an  average 
of  —2.62  nun.  Hg.  during  inspiration  and  +1.01  during  expiration. 
In  a  case  of  valvular  pneumothorax,  the  average  pressure  at  the 
height  of  inspiration  was  +7.93  mm.  Hg.,  during  expiration  +10.48. 
In  a  patient  with  closed  pneumothorax  the  pressure  in  inspiration  was 
+0.4,  in  expiration  +5.0.  A  positive  pressure  at  the  height  of  inspira- 
tion as  in  this  ease  suggests  the  diagnosis  of  closed  pneumothorax. 
Among  West's1  20  eases  of  pneumothorax  the  highest  pressure  was 
9  inches  of  water  (17  mm.  Hg.). 

Incidence. — The  cases  occur  more  commonly  in  early  adult  life, 
between  twenty  and  thirty,  corresponding  to  the  period  when  pul- 
monary tuberculosis  is  most  frequent.  The  condition  is  occasionally 
observed  in  children,  but  is  rare  under  three  years  of  age.  It  may 
occur  as  the  result  of  trauma  in  efforts  to  resuscitate  the  newborn. 
Males  are  more  frequently  affected,  probably  because  subjected  to 
greater  physical  exertion.  Among  Drasche's2  198  cases,  158  were 
males.  In  James'3  series  of  125  cases,  103  were  males.  Statistics 
vary  as  to  the  frequency  with  which  the  two  sides  are  affected.  It 
seems  to  be  somewhat  more  common  on  the  left. 

Etiology. — There  are  three  groups:  (1)  The  air  may  come  from  a 
perforation  of  the  pulmonary  pleura  and  the  lung,  bronchi,  trachea, 
esophagus,  stomach  or  intestines,  forming  an  internal  fistula.  (2)  Air 
may  gain  entrance  to  the  pleura  through  a  perforating  wound  of  the 
outer  chest  wall,  forming  an  external  fistula.  In  both  groups  atmos- 
pheric air  is  admitted  to  the  pleura.  (3)  Gas  may  be  generated  by 
decomposition  of  a  pleural  exudate  and  without  demonstrable  external 
or  internal  fistula. 

The  commonest  cause  is  disease  of  the  lung,  and  in  the  majority 
of  the  cases  there  is  tuberculosis.  Among  Biach's4  918  cases  from 
three  Vienna  hospitals  715  (77  per  cent.)  were  due  to  pulmonary 
tuberculosis.  Of  Weil's5  55  cases,  46  (84  per  cent.)  were  tuberculous. 
In  Drasche's6  230  cases,  198  (86  per  cent.)  were  ascribed  to  this  cause; 
of  Mosheim's7  50  cases,  42  (86  per  cent.).  Thus  from  SO  to  90  per 
cent,  may  be  regarded  as  tuberculous. 

The  incidence  of  pneumothorax  among  patients  with  pulmonary 
tuberculosis  was  36  (10.1  per  cent.)  among  355  cases  which  came  to 
autopsy  in  Weil's  series.  West8  estimates  it  as  5  per  cent,  of  the 
fatal  cases.  In  large  series  of  clinical  cases  the  proportion  is  lower, 
as  among  Drasche's9  10,212  cases  of  pulmonary  tuberculosis  in  which 
there  were  198  (1.93  per  cent.)  with  pneumothorax. 

1  Intrapleural  Tension,  Allbutt's  System  of  Medicine,  1899. 

2  Wien.  klin.  Woch.,  1899,  Nos.  45  and  46. 

3  Osier's  Mod.  Med.,  1st  ed.,  vol.  iii,  p.  870. 

A  Zur  Aetiologie  des  Pneumothorax,  Wien.  med.  Woch.,  1880,  vol.  xxx. 
5  Deut,  Arch.  f.  klin.  Med.,  May  30  and  July  13,  1882. 
c  Wien.  klin.  Woch.,  1899,  No.  45. 

7  Beitriige  z.  Klinik  der  Tub.,  1905,  vol.  iii. 

8  A  Contribution  to  the  Pathology  of  Pneumothorax,  Lancet,  May  3,  1881. 

9  Wien.  klin.  Woch.,  December  21,  1899,  No.  51. 


PNEUMOTHORAX  567 

Pneumothorax  occurs  more  often  in  active  than  in  latent,  inactive 
or  arrested  tuberculosis.  Most  cases  are  due  to  the  rupture  of  small 
subpleural  tubercles  which  break  down  before  communication  with 
the  pleural  cavity  is  prevented  by  the  formation  of  adhesions.  Its 
infrequency  in  connection  with  large  cavities  and  the  more  chronic 
types  of  the  disease  is  due  to  the  more  extensive  and  firmer  pleural 
adhesions  in  these  forms.  The  apex  of  the  lung,  though  the  most 
common  site  of  cavity  formation,  is  seldom  the  seat  of  the  rupture 
owing  to  the  frequency  with  which  pleural  adhesions  obliterate  the 
pleural  sac  in  this  region.  Rupture  of  the  pleura  may  occur  during 
a  violent  effort,  as  coughing,  lifting  or  sneezing,  but  in  many  cases 
there  is  no  apparent  immediate  cause  and  the  patient  may  be  at  rest 
in  bed.  In  23  cases  with  sudden  onset  at  the  Massachusetts  General 
Hospital  the  pneumothorax  occurred  while  the  patient  was  sitting 
still  or  in  bed  in  14. 

Of  other  diseases  of  the  lung  in  which  pneumothorax  may  occur, 
abscess  or  gangrene  and  bronchiectasis  as  a  group  stand  next  in  fre- 
quency, but  the  cases  are  rare.  Pulmonary  infarction  may  be  the 
underlying  cause.  Bach1  reports  3  cases  and  collected  31  from  the 
literature  in  which  emphysema  was  a  certain  or  probable  cause.  There 
were  15  autopsies,  and  pulmonary  tuberculosis  was  present  in  5. 
Tumors  of  the  lung  and  echinococcus  disease  are  rare  causes.  Abscess 
and  hydatid  disease  of  the  liver,  ulcer  or  cancer  of  the  stomach,  cancer 
of  the  esophagus,  and  perforation  of  the  esophagus  by  a  fish  bone  have 
been  recorded  as  causes  of  pneumothorax.  Spontaneous  erosion  and 
perforation  of  the  lung  or  the  chest  wall  by  an  empyema  in  rare  in- 
stances cause  pneumothorax. 

Pneumothorax  may  be  caused  by  a  penetrating  wound  of  the  chest 
wall  or  of  the  lung,  such  as  stab  or  gun-shot  wounds,  but  it  is  surprising 
how  seldom  this  complication  occurs.  Among  21  cases  of  penetrating 
wounds  of  the  chest  in  Bach's  series  there  were  no  instances  of  pneu- 
mothorax. Otis2  states  that  pneumothorax  was  a  troublesome  com- 
plication in  less  than  a  half  dozen  cases  among  the  vast  number  of 
chest  wounds  during  the  war.  In  fractures  of  the  ribs  a  fragment  of 
bone  may  injure  the  lung  and  produce  pneumothorax.  In  James' 
series  of  127  cases  11  were  due  to  this  cause.  Occasionally  a  marked 
concussion  of  the  body  may  rupture  the  lung  and  thus  cause  pneumo- 
thorax without  external  wound  or  fracture  of  a  rib.  Hemothorax 
is  a  frequent  complication  in  traumatic  pneumothorax.  Empyema 
operated  in  the  ordinary  way  is  converted  into  open  traumatic  pneu- 
mothorax. 

The  operation  of  thoracentesis  may  be  responsible.  A  considerable 
number  of  cases  have  been  reported.    Sears3  in  1906  was  able  to  find 

1  Ueber  das  Vorkommen  des  spontanen  Pneumothorax  bei  Emphysem,  Beitrage 
z.  Klinik  d.  Tub.,  1910-11,  xviii,  21. 

2  The  Medical  and  Surgical  History  of  the  War  of  the  Rebellion,  Part  I,  Vol.  I. 

3  Amer.  Jour.  Med.  Sci.,  1906,  cxxxii,  850. 


5GS  DISEASES  OF  THE  PLEURA 

references  to  50  eases.  Injury  to  the  lung  by  the  point  of  the  instru- 
ment is  rarely  a  cause.  Faulty  technic  and  the  entrance  of  air 
through  the  cannula  or  needle  is  common,  radiographic  examination 
not  infrequently  indicating  the  presence  of  pneumothorax  after  the 
partial  aspiration  of  pleural  fluid.  The  amount  admitted  in  this  way 
is  ordinarily  small  and  no  unfavorable  symptoms  usually  ensue.  The 
use  of  an  air-tight  trocar  diminishes  this  danger.  Misapplication  of 
the  tubing  to  the  aspirating  pump  of  Potain's  apparatus  so  that  air 
under  positive  pressure  is  blown  into  the  chest  has  caused  immediate 
death.  The  rupture  of  pleural  adhesions,  an  emphysematous  vesicle 
or  superficial  pulmonary  cavity  by  an  excess  of  negative  pressure 
during  the  aspiration  of  pleural  fluid  is  probably  the  most  common 
cause  of  the  more  serious  types  of  pneumothorax  in  this  group.  It 
has  been  assumed  that  the  reduction  of  pleural  pressure  by  aspiration 
may  liberate  gas  from  the  pleural  bloodvessels  and  give  rise  to  a  so- 
called  "pneumothorax  ex  vacuo."  Although  the  possibility  of  this 
must  be  admitted  in  a  cavity  with  rigid  walls,  yet  the  amount  of  gas 
must  be  small  and  of  no  practical  importance. 

There  is  a  small  group  of  cases  in  which  pneumothorax  occurs  in 
apparently  healthy  individuals  after  some  unusual  exertion,  at  times 
after  laughing,  crying,  coughing,  sneezing  or  yawning,  and  in  rare  in- 
stances while  at  rest  and  even  asleep.  There  may  be  nothing  in  the 
history  or  physical  examination  to  suggest  tuberculosis  and  the  pneu- 
mothorax is  rarely  complicated  by  an  effusion.  This  is  the  so-called 
spontaneous  or  idiopathic  pneumothorax.  Fussell  and  Riesman1 
reported  2  and  collected  56  cases  from  the  literature.  Young  adults 
are  most  frequently  affected.  Death  rarely  follows  and  the  pathology 
is  not  definitely  known.  Latent  tuberculosis,  the  rupture  of  an  emphy- 
sematous vesicle  or  the  tearing  of  pleural  adhesions  are  to  be  con- 
sidered in  explanation.  The  frequency  of  tuberculosis  as  a  cause 
of  other  types  of  pneumothorax  makes  it  necessary  to  exclude  it  more 
rigorously  than  has  hitherto  been  done  before  any  other  explanation 
can  be  accepted.  In  cases  in  which  other  evidence  of  tuberculosis 
is  lacking,  negative  tests  should  be  obtained  with  sufficiently  large 
doses  of  tuberculin  before  the  non-tuberculous  character  of  the  dis- 
turbance can  be  regarded  as  established. 

Finally  there  are  a  few  cases  in  which  pneumothorax  appears  to 
be  due  to  the  development  in  pleural  fluid  of  a  gas-producing  organ- 
ism. In  Levy's2  case,  Frankel's  anerobic  gas-producing  organism  was 
found;  in  May  and  Gebbard's3  case  an  unidentified  gas-producing, 
organism;  in  Hamilton's4  the  Bacillus  aerogenes  capsulatus;  and  in 
Findley's5  the  colon  bacillus. 

1  Amer.  Jour.  Med.  Sci.,  August,  1902. 

2  Arch.  f.  exper.  Path.  u.  Pharm.,  1895,  xxxv,  335. 
:i  Deut.  Arch.  f.  klin.  Med.,  1898,  vol.  Ixi. 

4  Montreal  Med.  Jour.,  December,  1898. 

5  Ibid.,  1899,  xxviii,  759. 


Pneumothorax  569 

Pathology. — If  there  are  no  pleural  adhesions  and  the  opening  into 
the  pleura  is  large,  the  lung  collapses  and  retracts  to  a  varying  degree 
toward  the  root  and  may  be  found  at  autopsy  as  a  more  or  less 
shrunken  mass  lying  against  the  spinal  column.  In  long  standing 
cases  it  may  be  tough,  fibrinous,  and  practically  airless  with  little  resem- 
blance to  the  normal  lung.  Areas  of  tuberculosis  with  cavity  forma- 
tion are  usually  present.  Pleural  adhesions  may  bind  the  lung  at  one 
or  more  places  to  the  chest  wall  over  a  greater  or  less  extent.  In  some 
instances  air  is  confined  to  a  portion  only  of  the  pleural  space,  giving 
rise  to  partial  pneumothorax.  Confinement  to  an  interlobar  space 
without  contact  with  the  periphery  of  the  lung  was  observed  at  autopsy 
in  the  case  reported  by  Monnier.1    Such  instances  are  extremely  rare. 

The  perforation  can  usually  be  demonstrated  without  trouble  and 
commonly  leads  into  a  large  or  small  tuberculous  cavity  at  the  periph- 
ery of  the  lung.  The  hole  may  be  several  centimeters  in  diameter 
or  so  small  as  to  be  visible  and  first  discovered  only  after  the  inflated 
lung  is  submerged  in  water.  The  perforation  is  usually  single,  but 
in  rare  instances  two  or  more  are  found.  In  Roe's2  case  a  left-sided 
pneumothorax  was  due  to  perforation  of  the  right  lung  through  an 
adherent  mediastinum.  In  some  instances,  an  inflammatory  exudate 
occludes  the  perforation,  converting  an  open  into  a  closed  pneumo- 
thorax. 

Experiments  on  animals  and  observations  on  man  have  shown 
that  air  alone  does  not  act  as  an  irritant  to  the  pleura,  but  since  pneu- 
mothorax usually  arises  under  conditions  in  which  bacteria  readily  gain 
entrance  to  the  pleura,  it  is  only  in  exceptional  instances,  such  as 
spontaneous  pneumothorax  or  in  rapidly  fatal  forms,  that  pleurisy 
fails  to  complicate  the  process.  A  fluid  exudate  usually  forms  and 
according  to  West3  is  serous,  seropurulent  or  purulent,  each  in  about 
one-third  of  the  cases.  Purulent  exudates  are  common  in  children 
and  following  rupture  from  the  alimentary  canal.  Hemothorax  is 
not  infrequent  in  traumatic  cases. 

Displacement  of  the  thoracic  and  abdominal  organs  takes  place  and 
usually  to  a  degree  proportional  to  the  amount  of  air  and  fluid  in  the 
pleura.  The  mediastinum  and  the  heart  are  moved  to  the  opposite 
side  unless  held  by  adhesions.  According  to  James'  observations  and 
contrary  to  the  general  impression,  the  heart  is  not  rotated  or  swung 
from  its  point  of  attachment  at  the  root  of  the  great  vessels,  but 
carried  bodily  across  to  the  opposite  side,  its  long  axis  maintaining 
about  its  normal  relation  to  the  long  axis  of  the  body.  Encroachment 
on  the  sound  lung  follows  the  displacement  of  the  mediastinum.  Dis- 
location of  the  heart  is  greater  with  left  than  with  right-sided  processes. 
The  diaphragm  is  depressed  on  the  affected  side  at  times  to  such  a 
degree  that  it  projects  downward  and  presents  a  convex  surface  toward 
the  abdomen  into  which  the  movable  viscera  are  also  crowded.     The 

1  Gaz.  med.  de  Nantes,  November  2,  1907. 

2  Med.  Times  and  Gaz.,  April  7,  1866.  3  Lancet,  1887,  i,  1264. 


570  DISEASES  OF  THE  PLEURA 

position  assumed  by  the  heart  and  abdominal  organs  is  well  shown 
in  the  accompanying  plates  from  photographs  taken  at  autopsy. 
(See  Plates  II  arid  III.) 

Symptoms.  Sudden  onset  is  relatively  uncommon.  In  OS  of 
Saussier's1  196  eases  it  was  with  violent  pain  and  dyspnea.  Of  04 
certainly  or  probably  tuberculous  cases  at  the  Massachusetts  General 
Hospital  the  onset  was  sudden  in  23.  Much  depends  on  the  local 
conditions.  The  initial  symptoms  are  most  severe  when  there  are 
no  pleural  adhesions  and  the  lung  and  mediastinum  are  free  from 
disease,  permitting  complete  collapse  of  the  lung  and  dislocation  of 
the  mediastinum  toward  the  sound  side.  The  most  alarming  onset 
is  therefore  likely  to  be  observed  in  early  tuberculous  cases,  in  trau- 
matic or  in  spontaneous  pneumothorax.  Noteworthy  symptoms  are 
usually  lacking  when  it  occurs  as  a  complication  of  empyema  rup- 
turing through  the  lung  or  following  thoracentesis  for  the  removal  of 
pleural  effusion. 

Symptoms  when  present  are  most  commonly  pain  in  the  affected 
side  and  sudden  and  severe  or  rapidly  progressive  dyspnea.  In  uncom- 
plicated cases  there  is  slight  and  unproductive  cough.  If  there  is 
considerable  purulent  material  in  an  infected  lung  more  abundant 
sputum  may  follow  its  expression  from  pulmonary  cavities  or  the 
bronchi.  The  rupture  may  be  felt  as  in  Stokes'2  case  or  it  may  be  even 
audible  to  the  patient  as  reported  by  Banks.3  The  symptom  complex 
may  simulate  angina  pectoris.  In  Beardsley's4  case  with  extensive 
left  pneumothorax  there  was  sharp,  severe  pain  with  muscular  spasm 
in  the  left  side  of  the  abdomen  suggesting  peritonitis,  but  none  was 
found  at  autopsy. 

A  typical  severe  attack  like  the  following  is  occasionally  observed. 
Thus,  in  a  person  previously  in  apparent  good  health  there  may  be 
sudden,  sharp  pain  in  the  chest,  an  immediate  intense  feeling  of  suffo- 
cation and  fear  of  impending  death,  air  hunger,  and  great  restless- 
ness; the  face  at  first  pale  and  later  cyanotic;  the  hands  and  feet 
cold  and  blue;  the  skin  bathed  in  cold  sweat.  The  alee  nasse  dilate, 
the  respirations  are  rapid,  and  the  accessory  muscles  of  respiration  are 
brought  into  play.  The  patient  is  usually  found  in  the  sitting  position 
and  if  able  to  speak  may  plead  in  a  weak  and  scarcely  audible  voice 
to  be  taken  to  the  open  window.  The  pulse  is  rapid,  small,  feeble, 
or  imperceptible.  In  5  of  83  cases  (Massachusetts  General  Hospital) 
the  attack  was  followed  by  unconsciousness,  which  terminated  in 
death  in  one  instance. 

In  milder  cases  there  may  be  only  slight  pain  and  an  increase  of 
dyspnea,  the  patient  meanwhile  not  being  incapacitated.  In  four 
cases  (Massachusetts  General  Hospital)  the  succussion  splash  was 
the  first  intimation  to  the  patient  and  the  principal  symptom  of  which 

1  Thesis,  Paris,  1841.  2  Diseases  of  the  Chest,  1837. 

3  Dublin  Quart.  Jour.  Mecl.  Sci.,  1854,  vol.  xvii. 

4  New  York  Med.  Jour.,  1911,  xciii,  529. 


PNEUMOTHORAX  571 

he  complained.  In  the  majority  of  cases  the  occurrence  of  pneumo- 
thorax leaves  no  striking  impression  on  the  clinical  aspect  or  is  indi- 
cated only  by  an  aggravation  of  existing  symptoms.  This  is  due  to 
its  usual  occurrence  late  in  the  course  of  pulmonary  tuberculosis  when 
the  lung  is  already  considerably  involved  and  the  pleural  sac  partially 
obliterated  by  adhesions.  In  many  cases  the  condition  is  unsuspected 
and  discovered  only  in  the  course  of  the  routine  physical  examination. 

Signs. — These  are  commonly  striking  and  distinctive.  Small 
amounts  of  air  may  readily  escape  detection,  however,  and  be  first 
noted  in  the  x-ray  examinations. 

Inspection. — Immediately  following  the  entrance  of  a  large  amount 
of  air  into  the  pleura  the  patient  usually  finds  the  sitting  or  half- 
sitting  position  most  comfortable.  In  rare  instances,  as  in  Garde's1 
remarkable  case  the  knee-elbow  position  is  assumed,  probably  to 
prevent  the  disturbances  incident  to  backward  displacement  of  the 
,  heart.  In  this  instance  it  was  maintained  for  about  fifty-six  days  (!). 
The  decubitus  in  the  more  severe  cases  is  likely  to  be  on  the  affected 
side.  Immobility,  distention,  flattening  or  fulness  of  the  intercostal 
spaces,  and  absence  of  the  diaphragm  shadow  may  be  noted.  Weil 
reported  edema  of  the  hand  on  the  affected  side,  Zahn,2  of  the  chest 
wall.  Subcutaneous  emphysema,  at  times  of  an  extreme  grade,  is 
occasionally  seen  in  traumatic  cases  or  following  thoracentesis.  Dis- 
location of  the  heart  away  from  the  affected  side  is  an  important 
early  sign  and  may  be  indicated  by  a  visible  cardiac  impulse  to  the 
right  or  left  of  its  normal  position,  the  displacement  being  most  marked 
in  left-sided  cases. 

Palpation. — Vocal  fremitus  is  much  diminished  or  abolished  over 
the  involved  region.  In  70  of  James'  series  in  which  this  was  noted 
above  the  level  of  fluid,  it  was  diminished  in  52  and  absent  in  18  cases. 
Vocal  fremitus  is  usually  absent  over  fluid.  With  a  large  amount  of 
air  the  intercostal  spaces  may  be  felt  to  be  wider  than  on  the  unaffected 
side.  Palpation  may  also  establish  the  position  of  the  displaced  cardiac 
impulse  and  that  of  the  depressed  liver  or  spleen.  Depression  and 
inversion  of  the  diaphragm  can  hardly  be  determined  by  palpation 
alone. 

Mensuration. — This  may  show  enlargement  of  the  affected  side;  but 
the  side  may  look  larger  and  this  fail  of  confirmation  with  the  tape  or 
the  affected  side  may  measure  less  than  the  other. 

Percussion. — The  percussion  note  is  largely  dependent  on  the  size, 
shape,  and  tension  of  the  air-holding  cavity,  the  position  of  the 
retracted  lung,  the  presence  of  adhesions,  character  of  the  pneumo- 
thorax, whether  open  or  closed,  and  the  presence  or  absence  of  fluid. 
The  condition  of  the  pleura  appears  to  have  no  striking  or  constant 
influence  on  the  percussion  sound  and  it  is  sometimes  difficult  or  im- 
possible to  explain  variation  in  different  cases  or  in  different  parts  of 

1  Arch.  gen.  de  Med.,  1828,  xvii,  345.  2  Virchow's  Arch.,  1891,  p.  123. 


572  DISEASES  OF  THE  PLEURA 

the  chest.  The  percussion  note  is  usually  strikingly  loud,  of  low  pitch, 
and  may  be  described  as  hyperresonant  and  such  as  is  obtained  over 
an  emphysematous  lung.  If  the  pneumothorax  is  large  and  the  pleura 
tree  from  adhesions  hyperresonance  may  be  determined  to  extend 
beyond  the  limits  of  the  normal  lung,  exceeding  the  middle  line  toward 
the  unaffected  side  over  the  mediastinum  and  invading  or  abolishing 
the  hepatic  or  splenic  dulness.  The  cardiac  dulness  also  disappears 
or  changes  its  position.  In  open  pneumothorax  there  may  be  a  tym- 
panitic note.  In  some  cases  the  resonance  is  defective  or  dull.  The 
percussion  note  may  have  an  amphoric  quality. 

With  total  pneumothorax,  the  retracted  lung  lies  along  the  spine 
and  is  not  demonstrable  by  percussion  but  if  adhesions  bind  it  over 
a  larger  or  smaller  extent  to  the  chest  wall  the  percussion  note  is 
impaired  over  the  adherent  area.  Defective  resonance  from  this 
cause  is  frequently  demonstrable  at  the  apex,  may  be  found  along  the 
spine  posteriorly,  and  at  times  in  other  parts  of  the  chest.  The  occa- 
sional presence  of  areas  of  tympanitic  resonance  below  the  level  of 
fluid  may  be  due  to  pleuritic  adhesions. 

Other  modifications  are  at  times  observed.  A  cracked-pot  sound 
may  be  obtained,  due  either  to  proximity  of  a  pulmonary  cavity  to 
the  chest  wall  or  communication  of  a  large  open  fistula  with  the  pleural 
cavity.  Inconstant  changes  in  the  percussion  note  with  the  mouth 
open  or  closed,  on  assuming  the  erect  or  recumbent  posture,  during 
inspiration  or  expiration,  and  before  or  after  aspiration  may  also  be 
noted. 

A  small  amount  of  pleural  fluid  complicating  pneumothorax  and 
concealed  in  the  hollow  of  the  diaphragm  may  not  be  demonstrable 
by  percussion  although  readily  detected  by  succussion.  Dulness  or 
flatness  is  generally  present  over  large  effusions  but  the  amount  is 
frequently  underestimated,  and  Skoda's  suggestion,  i.  e.,  to  estimate 
the  amount  of  fluid  in  pneumothorax  double  that  indicated  by  per- 
cussion, if  followed,  will  prevent  some  mistakes.  The  upper  level  of 
fluid  is  not  always  easy  of  determination  and  is  likely  to  be  placed 
too  low,  so  that  an  instrument  introduced  for  the  removal  of  air  may 
be  found  to  be  below  the  level  of  fluid.  Marked  mobility  of  the  dul- 
ness over  fluid  and  the  constant  maintenance  of  a  horizontal  upper 
border,  in  whatever  position  the  patient  is  placed,  are  important  and 
characteristic  features  of  pneumohydrothorax,  in  striking  contrast 
to  the  relative  immobility  and  curved  upper  limit  of  dulness  in  pleural 
effusions  without  air.  In  two  of  Emerson's  cases  with  a  large  amount 
of  fluid  a  small  amount  of  air  could  constantly  be  demonstrated  in 
the  uppermost  point  of  the  chest  with  the  patient  in  different  positions. 

Auscultation. — Suppressed  or  absent  breathing  combined  with  hyper- 
resonance  on  percussion  is  usually  the  first  indication  in  the  course 
of  the  examination  that  pneumothorax  exists,  and  this  diminution  in 
the  respiratory  murmur  is  the  more  striking  in  contrast  to  the  exag- 
gerated breath  sounds  over  the  uninvolved  lung.   Diminished  bronchial 


PNEUMOTHORAX  573 

breathing  may  also  be  heard.  The  voice  sounds  and  the  whisper  are 
diminished  or  absent.  Among  90  of  James'  cases  in  which  the  char- 
acter of  the  respiratory  murmur  was  noted  it  was  found  to  be  dim- 
inished in  41,  amphoric  in  31,  absent  in  12,  and  bronchial  in  6  cases. 

Amphoric  Phenomena. — The  breathing  not  infrequently  presents 
a  peculiar  metallic  quality  resembling  the  sound  produced  by  blow- 
ing over  the  mouth  of  an  empty  decanter  and  hence  spoken  of  as 
amphoric.  This  was  first  described  by  Laennec  as  "  bourdonnement 
amphorique,"  and  ascribed  to  the  motion  of  the  air  in  and  out  of  the 
pleural  cavity  through  an  open  fistula.  In  support  of  this  explana- 
tion it  may  be  said  that  an  open  fistula  exists  in  most  of  the  cases  in 
which  amphoric  breathing  is  heard  and  the  point  of  maximum  inten- 
sity of  the  amphoric  breathing  over  the  chest  is  occasionally  observed 
to  coincide  with  the  position  of  the  fistula  found  at  autopsy.  The 
factors  leading  to  the  production  of  this  sound  have  been  the  subject 
of  much  controversy  and  cannot  yet  be  regarded  as  settled.  The 
report  of  cases  by  Marechal,1  West2  and  Emerson3  in  which  amphoric 
respiration  was  present  yet  the  fistula  was  certainly  or  probably  closed, 
Powell's4  observation  of  amphoric  respiration  over  a  distended  stomach 
and  Hoover's5  finding  of  amphoric  respiration  over  a  loop  of  distended 
intestine  in  the  left  hypochrondrium  suggest  that  a  communication 
with  the  pleural  cavity  is  unnecessary.  The  most  probable  explana- 
tion seems  to  be  that  the  sound  is  due  to  the  resonating  properties 
of  the  pneumothorax  cavity  and  is  produced  by  the  vibration  of  air 
within  the  cavity  itself  or  by  vibrations  propagated  from  neighboring- 
parts  of  the  lung  or  bronchial  tree.  The  presence  of  fluid  is  unneces- 
sary for  its  production.  It  is  variable  in  its  location,  intensity  and 
pitch.  Not  only  the  respiratory  murmur,  but  also  in  occasional 
instances  the  percussion  note,  cough,  vocal  resonance,  whisper,  the 
heart  sounds,  rales,  pleural  friction  and  deglutition  sounds  may  have 
a  metallic  and  amphoric  quality. 

Metallic  Tinkle. — This  is  impressive  and  characteristic,  and  de- 
scribed by  Laennec  as  resembling  the  sound  produced  by  gently  strik- 
ing with  a  pin  or  dropping  sand  into  a  glass,  metal,  or  porcelain  vessel; 
or  like  the  vibration  of  a  metallic  cord  touched  by  the  finger.  Several 
explanations  of  this  curious  phenomenon  have  been  offered.  Agita- 
tion of  the  fluid  against  the  walls  of  the  pleural  cavity,  the  bursting 
at  the  surface  of  fluid  of  bubbles  of  air  which  enter  through  a  sub- 
merged fistula,  the  falling  of  drops  from  the  walls  of  the  cavity  above  to 
the  surface  of  the  fluid  below  or  the  modification  by  a  suitable  reson- 
ance chamber,  such  as  the  pneumothorax  cavity,  of  rales  produced 
in  its  vicinity  have  been  suggested.  The  finding  of  metallic  tinkling 
in  cases  in  which  from  the  absence  of  the  succussion  splash  there  was 

1  Jour,  hebdom.  de  med.,  Paris,  1829,  vol.  ii. 

2  Trans.  Clin.  Soc,  London,  1884,  vol.  xvii. 

3  Johns  Hopkins  Hosp.  Rep.,  1903,  vol.  ii. 

4  Lancet,  March  4,  1882.  b  Cleveland  Jour,  of  Med,,  February,  189S. 


574  DISEASES  OF   THE  PLEURA 

reason  to  believe  that  fluid  was  absent,  as  in  those  reported  by  Finney1 
and  Maillart  and  Laserre2  lends  support  to  the  last  mentioned  view, 

but  as  small  amounts  of  fluid  may  fail  to  give  this  sign  this  explanation 
cannot  be  accepted  without  more  conclusive  evidence  of  the  absence  of 
Hind.  The  failure  of  Forbes3  to  find  on  dissection  any  communication 
between  the  bronchi  and  the  pleural  fluid  in  a  case  in  which  metallic 
tinkle  was  most  distinct  suggests  that  the  open  fistula  is  unnecessary. 
The  sound  may  be  heard  during  respiration,  speaking  or  coughing 
or  after  change  of  position.  In  some  instances  a  cough  may  be  needed 
to  produce  it  and  in  doubtful  cases  this  should  be  tried.  At  times  metal- 
lic tinkling  is  audible  to  the  patient  and  in  Allbutt's4  remarkable  case 
it  could  be  heard  for  two  hours  in  all  parts  of  a  large  room.  In 
James'  series  it  was  present  in  30,  absent  in  5  of  35  cases.  Amphoric 
breathing  may  or  may  not  be  present  with  it.  The  sign  is  not  dis- 
tinctive of  pneumothorax  but  may  be  heard  also  over  large  pulmonary 
cavities.  Herard5  heard  metallic  tinkling  over  a  dilated  kidney  con- 
taining pus  and  gas.     The  ureter  was  patent. 

Unverricht6  described  a  peculiar  phenomenon  heard  after  with- 
drawal of  part  of  the  air  in  pyopneumothorax.  With  each  inspiration 
there  were  sounds  like  those  heard  on  smoking  a  Turkish  water  pipe 
('^Yasserpfeifengerausch")  and  ascribed  to  the  bursting  at  the  sur- 
face of  the  fluid  of  bubbles  entering  through  an  open  pulmonary 
fistula.  Riegel  (quoted  from  Unverricht)  heard  a  similar  sound, 
unassociated  with  aspiration  and  only  when  the  patient  assumed 
such  a  position  that  the  fistula  opened  under  the  fluid. 

Succussion  Sound. — In  the  works  formerly  ascribed  to  Hippocrates 
it  is  recommended  "Seat  him  on  a  seat  which  will  not  stir.  Let  some 
one  hold  him  by  the  arms  while  you  shake  him  by  the  shoulders  and 
listen  to  hear  on  which  side  the  sound  is  produced."  The  sound  resem- 
bles that  produced  by  shaking  a  flask  half  full  of  water,  and  like  other 
sounds  heard  in  the  chest  in  the  presence  of  pneumothorax  may  have 
a  metallic  or  amphoric  quality.  It  is  the  earliest  and  most  important 
indication  of  the  presence  of  fluid  and  gas  in  the  pleural  cavity  and 
may  be  obtained  long  before  fluid  can  be  demonstrated  by  other 
means.  Small  amounts  of  fluid  may  fail  to  give  the  splash.  Its  inten- 
sity is  variable.  It  may  be  heard  only  by  the  most  attentive  ausculta- 
tion, readily  audible  to  the  examiner  and  even  to  the  patient 
or  in  some  instances  appreciated  in  all  parts  of  a  large  amphitheatre, 
as  in  James'  case  of  left  pyopneumothorax  (Plate  III).  At  times  it 
may  be  heard  only  with  the  patient  erect,  or  again  only  in  the  recum- 
bent position.  In  54  of  James'  cases  in  which  it  was  mentioned  it  was 
present  in  41,  absent  in  13  cases.     Similar  splashing  sounds  may  be 

1  Dublin  Jour,  of  Med.  Sci.,  April,  1898. 

2  Rev.  med.  de  la  Suisse  Rom.,  November  20,  1902. 

3  Translation  of  Laennec's  De  l'Auscultation  Med.,  1834. 

4  See  Finlay,  Pneumothorax,  Allbutt's  System  of  Med.,  1899,  vi,  378. 

5  Bull,  de  la  Soc.  Anat.,  1850,  xxv,  98.  6  Deut.  Klinik,  1903-07,  p.  208. 


PNEUMOTHORAX  575 

obtained  from  the  stomach,  the  intestine  or  the  peritoneum  if  fluid 
and  air  are  present,  but  the  site  of  maximum  intensity  and  other 
clinical  evidence  will  usually  serve  to  exclude  errors  from  these  sources. 
In  some  instances  it  may  be  necessary  to  be  sure  that  the  stomach 
is  empty  when  the  test  is  made.  The  churning  "mill-wheel"  mur- 
mur of  pneumohydropericardium  can  hardly  be  a  cause  of  confusion. 
Some  difficulty  is  occasionally  experienced  in  differentiating  pneu- 
mohydrothorax  from  a  pulmonary  cavity  containing  air  and  flu  id. 

Coin  Sound. — This  is  known  also  as  the  bell  sound  and  Bruit 
d'Arain.  It  was  first  described  in  an  anonymous  article,1  which 
attributes  its  discovery  to  Trousseau.  The  test  is  usually  made 
by  having  an  assistant  place  on  the  front  or  back  of  the  chest  a  coin 
against  which  another  coin  is  struck,  while  the  examiner  listens  with 
the  ear  or  the  stethoscope  at  a  point  on  the  chest  wall  directly  opposite. 
If  present,  a  clear,  musical,  bell-like  tone  is  produced,  resembling  in 
its  quality  the  amphoric  phenomena  previously  described  and  quite 
different  from  the  sound  obtained  for  comparison  over  the  unaffected 
side.  Among  25  of  Emerson's  cases  in  which  it  was  mentioned  it  was 
present  in  20,  absent  in  3,  suggestive  in  2.  In  37  of  James'  series,  it 
was  present  in  25,  absent  in  12.  This  sound,  like  amphoric  breathing, 
is  probably  due  to  the  peculiar  resonating  qualities  of  the  pneumo- 
thorax cavity.  It  is  not  absolutely  distinctive  of  pneumothorax. 
Osier2  reported  its  presence  over  a  large  cavity  in  the  right  upper  lobe. 

Gas  Analysis. — In  his  experiments  on  dogs,  Emerson  found  that  if 
air  be  introduced  into  the  chest  there  is  an  almost  immediate  accumu- 
lation of  C02  and  diminution  of  O  in  the  pleura,  but  the  N  remains 
remarkably  constant  until  a  point  is  reached  at  which  one  may 
suppose  that  absorption  is  well  under  way,  when  the  N  rises  about 
8  per  cent,  and  then  remains  quite  constant.  The  composition  depends 
on  the  gases  of  the  blood  and  on  the  local  respiration  of  the  tissues. 
Ewald3  determined  in  man  that  the  percentage  of  C02  is  greater  in 
the  presence  of  an  inflamed  pleura  and  greatest  when  there  is  pus. 
Analysis  of  the  gas  is  of  little  assistance  in  judging  the  condition  of 
the  fistula,  but  an  increasing  amount  of  oxygen  in  portions  of  gas 
successively  removed  suggests  an  open  fistula  as  in  Leconte  and  Demar- 
quay's4  case. 

Air  or  gas  which  has  gained  entrance  to  the  pleural  cavity  is  ab- 
sorbed, the  rate  of  absorption  varying  with  the  condition  of  the  pleura 
and  the  composition  of  the  gas.  Absorption  is  most  rapid  when  the 
pleura  is  normal.  According  to  Szupak's5  investigations  on  dogs 
atmospheric  air,  O  and  C02  are  absorbed  at  about  the  same  rate,  while 
N  is  taken  up  only  about  one-half  as  rapidly.    In  his  review  of  clinical 

1  Pneumothorax,  Nouveau  signe  pathognomique  de  cette  affection,  Gaz.  des  Hop., 
April  4,  1857. 

2  Montreal  Med.  Jour.,  1895,  xxiv,  969. 

3  Arch.  f.  Anat.  u.  Physiol.,  1876,  p.  422. 

4  Gaz.  med.  de  Paris,  1863,  third  section  1,  xviii,  114. 

6  Experimentelle  Untersuchungen  iiber  den  Pneumothorax,  Dorpat,  1891. 


576 


DISEASES  OF   THE  PLEURA 


Fig.  91 


Pneumothorax  of  right  side  following  stiletto  wound.     Retracted  lung  appears  as 
dense  shadow  at  lung  root.      (Dr.  W.  J.  Dodd.) 


Fig.  92 


Pneumothorax  of  the  right  side.  Displacement  of  the  heart  to  the  left.  Note  the 
definition  of  the  ribs,  the  clearness  of  the  intercostal  spaces  and  the  absence  of  the 
normal  lung  markings  on  the  right  in  comparison  with  the  left  side.  The  collapsed 
lung  is  seen  as  a  dense,  sharply  outlined  shadow  in  the  mid-chest.  Pleural  adhesions 
probably  account  for  the  failure  of  the  apical  portion  of  the  right  lung  to  completely 
collapse.  In  the  first  right  interspace  is  seen  a  small,  dense,  round  shadow  which  prob- 
ably represents  a  calcified  area  of  tuberculosis.    (Private  case  of  Dr.  L.  H.  Newburgh's.) 


I'NKUMOniOHAX 


577 


cases  he  finds  that  the  time  required  for  absorption  in  cases  without 
friction  rub  or  fluid  exudate  was  from  twenty-six  days  to  two 
months.  In  one  case  the  air  was  absorbed  in  six  days  and  in  another 
after  three  years.  The  possibility  of  slow  leakage  of  air  through  the 
fistula  or  of  inhibition  from  inflammation  of  the  pleura  must  be  con- 
sidered and  are  probably  largely  responsible  for  wide  differences  in 
the  apparent  rate  of  absorption. 

Fig.  93 


Pneumopyothorax  of  the  right  side.  The  fluid  is  indicated  by  the  opaque  shadow  with 
horizontal  upper  border.  Displacement  of  the  heart  to  the  left.  The  presence  of  air 
above  the  fluid  is  indicated  by  the  clearness  of  the  intercostal  spaces  and  the  absence 
of  the  normal  lung  markings.  The  collapsed  lung  is  seen  as  a  less  dense,  sharply  out- 
lined shadow  with  vertical  margin  above  the  fluid.     (No.  188,816.) 


X-ray  Examination. — This  not  only  serves  to  confirm  the  results  of 
physical  examination  but  may  show  small  collections  of  air  not  other- 
wise to  be  detected.  Both  the  fluoroscope  and  the  radiograph  should 
be  used.  Examination  in  the  erect  posture  is  usually  most  satis- 
factory. The  position  of  the  displaced  heart,  fracture  of  the  ribs, 
and  depression  of  the  diaphragm  may  be  noted.  An  accumulation 
of  air  is  seen  as  an  abnormally  clear  zone,  over  which  the  normal 
lung  markings  are  absent  and  the  ribs  more  sharply  defined  than 
at  other  parts  of  the  chest.  For  the  detection  of  small  bubbles 
of  air  above  pleural  effusions  Kraus  recommends  examination  with 
37 


578  DISEASES  OF   THE  PLEURA 

the  body  inclined  at  an  angle  of  about  45  degrees  and  finds  that  air 
can  thus  be  detected  when  nothing  is  seen  in  the  erect  position.  The 
collapsed  lung  is  seen  as  a  relatively  dense,  sharply  limited,  irregularly 
oval  shadow  in  the  niid-ehcst,  in  the  region  of  the  root  of  the  lung. 
An  incompletely  retracted  normal  lung  is  less  dense.  Infiltration  of 
the  tissue  may  be  responsible  for  failure  to  retract  and  may  add  to  the 
density  of  the  shadow.  Adhesions  may  account  for  irregularities  in 
the  contour  of  the  lung  and  appear  as  linear  or  band-like  connections 
between  the  lung  and  the  chest  wall.  Inspection  of  the  other  lung 
may  disclose  suggestive  evidence  of  tuberculosis. 

The  presence  of  pleural  fluid  adds  much  that  is  interesting,  instruc- 
tive, and  distinctive  to  the  picture.  It  appears  as  an  opaque  shadow 
at  the  bottom  of  the  chest  and  what  is  most  significant,  with  its  upper 
border  constantly  horizontal,  independent  of  the  patient's  position. 
With  the  patient  upright  the  upper  border  is  transverse.  When  he 
lies  on  his  side  it  is  parallel  to  the  long  axis  of  the  body.  The  upper 
border  is  most  sharply  defined  when  the  tube  is  in  line  with  the  level 
of  the  surface  of  fluid.  Examination  with  the  fluoroscope  shows  a 
wavy  motion  of  the  surface  on  shaking  the  patient,  tapping  the  abdo- 
men with  the  fingers,  percussion  of  the  chest,  or  during  cough.  Care- 
ful inspection  when  the  patient  is  still  discloses  also  a  depression  of 
the  level  of  the  fluid  during  expiration  and  elevation  during  inspira- 
tion, a  paradoxical  phenomenon  probably  due  to  lack  of  diaphragmatic 
tone  on  the  affected  side,  in  consequence  of  which  respiratory  changes 
in  abdominal  pressure  are  transmitted  to  the  fluid.  Inspiratory 
elevation  and  expiratory  depression  from  contraction  of  a  dia- 
phragm which  is  inverted  and  convex  below  seems  a  less  likely  expla- 
nation. Still  another  motion  is  synchronous  with  cardiac  systole, 
coincident  with  which  very  small  waves  start  from  the  mediastinal 
region  and  travel  across  the  surface  to  the  chest  wall. 

Varieties. — Open  Pneumothorax. — In  this  the  mechanical  relations 
are  simple.  An  open  fistula  connects  the  pleura  with  the  outside  air 
and  atmospheric  pressure  exists  in  the  pleural  space  with  respiratory 
oscillations  about  the  zero  point.  If  the  fistula  is  wide  open  the  col- 
lapsed lung  takes  little  or  no  part  in  respiration  and  the  intrapleural 
pressure  remains  nearly  constant  at  zero.  If  the  fistula  is  small  the 
respiratory  oscillations  are  greater  and  the  pressure  may  become  nega- 
tive in  inspiration  and  positive  in  expiration.  In  order  to  maintain 
its  patency  the  fistula  in  the  collapsed  lung  must  usually  be  large, 
with  rigid  walls,  and  run  in  a  direction  perpendicular  to  the  pulmonary 
surface;  hence  it  is  uncommon  as  a  result  of  perforation  of  the 
lung,  but  occurs  more  often  in  advanced  pulmonary  tuberculosis, 
occasionally  in  empyema  rupturing  through  the  bronchi,  and  may 
follow  thoracotomy. 

Respiratory  embarrassment  is  due  to  collapse  of  the  lung  and  dis- 
placement downward  of  the  diaphragm  and  of  the  mediastinum  toward 
the  sound  side.     Mediastinal  displacement  limits  the  excursion  of 


PNEUMOTHORAX  579 

the  sound  lung  and  the  efficiency  of  respiration.  Instability  of  the 
mediastinum  aggravates  the  symptoms.  If  free  to  move,  it  is  drawn 
toward  the  sound  side  during  inspiration  and  moves  toward  the 
affected  lung  during  expiration,  in  consequence  of  which  a  part  of 
the  expired  air  may  be  forced  into  the  collapsed  lung.  During  inspira- 
tion air  is  drawn  not  only  from  without  into  the  trachea  but  also  from 
the  collapsed  lung.  The  oscillation  from  one  lung  to  the  other  of  a 
volume  of  used  air,  the  so-called  "pendulum-air"  of  Brauer,  still 
further  reduces  the  efficiency  of  respiration.  During  forced  expira- 
tion with  cough,  inflation  of  the  collapsed  lung  is  increased. 

Valvular  Pneumothorax. — This  is  the  commonest  form  and  is  due  to 
valve-like  action  of  the  fistula,  which  permits  entrance  of  air  into  the 
pleura,  but  prevents  its  escape.  Rupture  of  a  small  pulmonary  cavity 
may  connect  the  bronchi  and  pleura  by  way  of  a  long,  narrow,  sinuous 
passage.  Inspiration  inflates  the  partially  collapsed  lung  and  draws 
air  into  the  pleural  cavity,  but  with  the  collapse  of  the  lung  during 
inspiration  the  fistula  is  closed  by  apposition  of  its  walls  and  the 
imprisoned  air  cannot  escape.  The  deeper  the  inspiration  the  more 
air  enters.  Cough  with  closed  glottis  greatly  increases  intrapulmonary 
pressure,  inflates  the  collapsed  lung,  opens  the  fistula,  and  further  dis- 
tends the  pleura.  Tuberculosis  is  the  cause  in  a  large  proportion  of 
such  cases. 

The  high  degree  of  pressure  which  may  be  produced  makes  this 
form  especially  dangerous  and  encroachment  on  thoracic  space  and 
dislocation  of  the  mediastinum  may  become  extreme,  with  displace- 
ment of  the  heart,  kinking  of  the  great  vessels,  narrowing  of  the 
principal  bronchi  and  diminished  volume,  elasticity,  and  effectiveness 
of  the  sound  lung.  Mobility  of  the  mediastinum  increases  the  danger 
and  thus  the  condition  is  more  serious  in  young  and  healthy  persons. 
The  outcome  depends  on  the  behavior  of  the  fistula.  Total  collapse 
of  the  lung  favors  healing  of  the  fistula,  but  at  times  after  partial 
absorption  of  air  and  reinflation  of  the  lung  the  fistula  again 
opens. 

Pneumothorax  Acutissimus. — This  is  also  known  as  suffocative 
pneumothorax  and  the  term  is  applied  to  cases  in  which  death  results 
within  a  few  hours.  A  valvular  fistula  with  the  rapid  development  of 
a  high  positive  pressure  or  grave  complications  in  the  lung  or  other 
organs  may  be  responsible. 

Closed  Pneumothorax. — This  is  only  a  phase  of  the  open  or  the  val- 
vular form  and  is  favorable,  since  closure  of  the  fistula  is  the  neces- 
sary forerunner  of  recovery.  The  orifice  of  the  fistula  may  be  sealed 
by  pleural  inflammation  or  adhesion  and  union  of  the  walls  of  the 
fistula.  Collapse  of  the  lung  favors  closure  of  the  fistula  and  small 
perforating  wounds  or  slight  pulmonary  lesions  in  a  comparatively 
healthy  lung  may  readily  close  in  this  way.  This  form  is  common 
in  spontaneous  pneumothorax,  in  relatively  early  tuberculous  cases 
and  after  thoracentesis. 


581)  DISEASES  OF  THE  PLEURA 

Double  Pneumothorax. — This  is  uncommon.  Death  usually  follows 
within  a  i'cw  hours.  Life  can  he  maintained  only  when  the  collapse 
of  one  or  both  lungs  is  incomplete.  Hellin1  has  collected  a  number 
of  cases. 

Partial  Pneumothorax. — In  this  form  adhesions  limit  the  air  to  a 
circumscribed  area.  Any  portion  of  the  pleural  sac  may  be  the  site. 
An  apical  localization  may  readily  lead  to  confusion  with  a  pulmonary 
cavity.  Monnier's2  case  in  which  the  position  of  the  pneumothorax 
in  the  interlobar  septum  was  proved  by  autopsy  is  of  especial  interest 
because  of  its  rarity. 

Artificial  Pneumothorax. — In  1882,  Forlanini3  suggested  the  possibil- 
ity of  treating  pulmonary  tuberculosis  by  establishing  artificial  pneu- 
mothorax on  the  affected  side  and  in  1894  reported  that  he  had  used 
the  method  and  described  his  technic.  In  1898,  Murphy4  reported 
5  cases  thus  treated.  The  method  attracted  little  attention  and 
received  no  encouraging  support  until  within  the  last  few  years,  during 
which  a  rapidly  increasing  number  of  publications  have  appeared. 
Forlanini5  has  recently  considered  the  method  at  length  and  reviewed 
the  literature. 

Theories. — The  method  is  based  on  the  assumption  that,  as  for 
tuberculous  processes  elsewhere,  immobilization  is  favorable  for  the 
arrest  of  a  tuberculous  process  in  the  lung  and  may  be  secured  by  the 
insufflation  of  pure  nitrogen  into  the  pleural  sac  on  the  diseased  side, 
this  gas  being  used  because  of  the  slowness  with  which  it  is  absorbed. 
Compression  of  the  lung  is  also  regarded  as  an  important  factor,  by 
diminishing  the  size,  evacuating  the  contents  and  approximating  the 
walls  of  pulmonary  cavities,  lessening  the  amount  of  infectious  material 
and  thus  retarding  the  activity  of  the  tuberculous  process.  Changes 
in  the  lymph  circulation  following  the  compression  are  supposed  to 
diminish  the  absorption  of  toxic  material  and  favor  the  development 
of  connective  tissue. 

Concerning  the  effects  of  the  immobilization  and  compression  of 
one  lung  upon  the  other,  which  must  of  necessity  work  harder,  it  is 
further  assumed  that  the  tuberculous  lesions,  almost  invariably  present 
although  of  less  extent,  are  favorably  affected  by  an  increase  in  res- 
piration, blood  and  lymph  circulation,  and  improvement  in  nutrition. 

Indications. — This  method  is  regarded  as  indicated  in  cases  -of 
pulmonary  tuberculosis,  after  unsuccessful  trial  of  other  wrell-known 
methods,  and  in  unilateral  cases  with  freedom  of  the  pleura  from 
adhesions.  Some  would  include  the  predominantly  unilateral  cases 
with  slight  and  relatively  inactive  processes  in  the  opposite  lung. 
The  treatment  is  also  recommended  for  intractable  hemoptysis  when 

1  Mitt.  a.  d.  Grcnzgeb.  d.  Med.  u.  C'hir.,  1909,  vol.  xvii. 

2  Gaz.  med.  dc  Nantes,  November  2,  1907. 

3  Gaz.  d.  osp.,  1882,  vol.  iii;    Gaz.  med.  di  Torino,  1894,  vol.  lxv. 

4  Jour.  Amer.  Med.  Assoc,  1898,  vol.  xxxi. 

6  Ergebnisse  der  inneren  Med.  u.  d.  Kinderheilk,  1912,  ix,  G21. 


PNEUMOTHORAX  581 

its  source  from  one  or  the  other  lung  can  be  determined  with  tolerable 
certainty.  Selected  cases  of  bronchiectasis  and  pulmonary  abscess 
or  gangrene  are  also  considered  suitable.  Obliteration  of  the  pleural 
sac,  acute  bilateral  processes  and  grave  cardiac  or  renal  lesions  are 
looked  upon  as  contra-indications.  An  .r-ray  examination  is  a 
necessary  preliminary  in  the  selection  of  cases. 

Apparatus. — The.  apparatus  used  by  Forlanini1  or  its  modifications 
by  different  workers2  consists  of  two  glass  receptacles  connected  by 
glass  or  rubber  tubing.  Out  of  one  receptacle  nitrogen  can  be  forced 
into  the  pleural  sac  by  water  or  air  pressure  in  the  other,  the  water 
meanwhile  acting  as  a  seal  to  prevent  the  escape  of  nitrogen  in  other 
than  the  right  direction.  A  manometer  is  so  arranged  that  it  can  be 
brought  into  or  out  of  connection  with  the  nitrogen  system  and  the 
pleura.  A  special  needle  is  used  for  the  puncture.  The  nitrogen  should 
be  chemically  pure  and  filtered  through  cotton  on  its  way  to  the  chest. 

Methods.- — In  choosing  the  site  for  the  injection,  freedom  from  pleural 
adhesions  is  the  most  important  determining  factor  and  the  injection 
is  made  wherever  the  pleura  seems  most  likely  to  be  free,  although 
the  lower  parts  of  the  chest  least  covered  with  muscular  tissue  are 
regarded  as  points  of  election.  Freedom  of  the  pleura  from  such  a 
degree  of  adhesions  as  would  be  likely  to  prevent  the  production  of 
pneumothorax  is  suggested  by  mobility  of  the  pulmonary  margin  over 
a  part  or  the  whole  of  its  extent  as  determined  by  axray  examination, 
percussion  of  the  complementary  space  during  forced  inspiration  and 
expiration,  and  observation  of  the  diaphragm  shadow.  Diminution 
in  amplitude  or  total  absence  of  respiratory  motion  suggest  partial 
or  complete  obliteration  of  the  pleura,  but  may  also  be  due  to  such 
other  causes  as  immobility  of  the  lung  from  disease,  weakness  of  the 
respiratory  muscles,  and  increased  intra-abdominal  pressure.  A 
history  of  pleurisy  on  the  affected  side,  lobar  pneumonia  as  a  cause  of 
the  process  or  pleural  pain  during  the  development  of  the  disease 
may  suggest  pleural  adhesions. 

In  the  performance  of  the  injection,  two  methods  are  in  use:  in  the 
Murphy-Brauer  method,  preceding  the  first  injection  an  incision  is 
made  to  the  parietal  pleura  through  which  the  needle  is  obliquely 
introduced,  in  that  of  Forlanini,  thoracentesis  is  performed  without 
preliminary  incision.  The  incision  method  diminishes  the  danger  of 
puncture  of  the  lung  and  gas  embolism,  but  is  likely  to  result  in  a 
greater  or  less  degree  of  subcutaneous  emphysema.  After  the  first 
injection  it  is  customary  to  give  subsequent  treatments  by  the  punc- 
ture method. 

Preceding  the  puncture  the  skin  should  be  frozen  with  ethyl  chlorid. 

1  Apparate  und  Operationstechnik  fur  den  kunstlichen  Pneumothorax,  Deut.  med. 
Woch.,  December  14  and  21,  1911.  For  detailed  descriptions  of  the  apparatus  the 
reader  is  referred  to  the  article  quoted. 

2  Robinson  and  Floyd,  Arch.  Int.  Med.,  1912,  ix,  452;  Balboni,  Med.  Comm.  of  the 
Mass.  Med.  Soc,  1912,  vol.  xxiii. 


582  DISEASES  OF  THE  PLEURA 

The  skin  and  underlying  tissues  are  then  thoroughly  anesthetized  with 
I  per  cent,  novocain,  containing  1  to  10,000  adrenalin  (Robinson). 
The  needle,  unconnected  with  the  apparatus  and  with  the  stop-cock 
on  the  lateral  outlet  closed,  is  introduced  to  what  seems  a  proper 
depth,  the  trocar  is  removed,  and  the  needle-cock  closed.  The  needle 
is  now  connected  with  the  manometer  of  the  apparatus,  the  nitrogen 
system  meanwhile  remaining  closed.  The  position  of  the  point  of  the 
needle  just  within  the  two  layers  of  the  pleura  is  indicated  by  the 
appearance  of  negative  pressure  and  marked  respiratory  oscillations  in 
the  manometer,  in  the  absence  of  which  it  is  never  safe  to  proceed 
with  the  injection,  which  must  be  abandoned  or  another  site  chosen. 
If  the  point  of  the  needle  is  in  the  thoracic  wall,  in  a  bloodvessel  or 
in  an  adherent  pleura,  negative  pressure  and  respiratory  oscillations 
are  absent,  if  in  the  lung,  respiratory  oscillations  may  be  present  but 
there  will  be  no  constant  negative  pressure.  If  the  point  of  the  needle 
lies  in  the  endothoracic  fascia,  slight  negative  pressure  and  respiratory 
oscillations  may  be  present.  Aspiration  by  means  of  a  syringe 
attached  to  the  needle  may  help  to  exclude  the  possibility  of  punc- 
ture of  a  vein. 

If  the  desired  negative  pressure  and  respiratory  oscillations  are 
obtained,  the  manometer  is  excluded  and  the  nitrogen  system  brought 
into  connection  with  the  needle,  through  which  nitrogen  is  allowed  to 
flow  into  the  pleural  sac  under  very  slight  pressure,  to  an  amount 
varying  usually  from  50  to  500  c.c.  Small  amounts  are  reinjected  at 
intervals,  commonly  at  first  each  week.  The  amount  and  frequency 
are  determined  by  the  conditions  in  individual  cases,  the  indi- 
cation being  to  maintain  the  affected  lung  completely  immobile. 
Distress  or  pain  during  the  injection  indicates  a  dangerous  degree  of 
tension  on  adhesions  and  makes  it  wise  to  terminate  the  procedure. 
The  length  of  time  over  which  the  treatment  is  to  be  carried  out  can- 
not be  definitely  stated  and  will  depend  on  the  result  obtained.  It 
has  been  maintained  for  as  long  as  ten  years  in  one  of  Forlanini's 
cases. 

In  cases  in  which  there  is  reason  to  believe  there  may  be  pleural 
adhesions  at  the  site  of  the  puncture,  Forlanini  is  not  deterred,  but 
believes  that  the  procedure  can  be  accomplished  by  a  modified  tech- 
nic.  The  adherent  pleural  space  cannot  be  detected  in  the  manner 
already  described  and  the  nitrogen  must  be  introduced  under  pressure 
to  forcibly  separate  the  adhesions.  With  the  needle  in  place  minimal 
amounts  of  nitrogen  are  injected  by  pressure  upon  the  rubber  tubing. 
By  pressure  with  the  thumb  and  forefinger  of  the  right  hand  the  tube 
is  closed  at  a  point  about  3  cm.  from  the  connection  with  the  needle. 
Compression  of  the  short  section  of  tubing  thus  isolated  with  two 
fingers  and  the  thumb  of  the  left  hand  expresses  from  the  point  of  the 
needle  about  one-half  cubic  centimeter  of  nitrogen.  If  pressure  on 
the  tubing  is  now  released  and  the  tension  tested,  the  behavior  of  the 
manometer  will  disclose  the  presence  of  the  expressed  nitrogen  in  a 


PNEUMOTHORAX  583 

closed  vesicle  within  the  tissue,  its  more  diffuse  distribution  between 
the  layers  of  the  pleura  or  entrance  into  a  vessel.1 

Dangers. — Embolism  is  the  most  immediate  danger  and  when  it 
occurs  is  commonly  fatal  if  large  amounts  of  gas  have  entered  a  vein. 
Of  98  cases  treated  by  Forlanini,  this  accident  occurred  with  a  fatal 
result  in  2  during  a  repetition  of  the  injection.  Three  fatal  cases 
by  the  puncture  method  were  reported  to  Brauer2  by  other  operators 
and  1  occurred  in  his  own  experience.  Many  isolated  examples  are 
reported  in  the  literature.  Hemiplegia  has  followed.  Sudden  death 
apparently  due  to  irritation  of  the  pleura  ("eclampsic  pleurisy") 
is  occasionally  observed,  but  may  follow  puncture  of  the  pleura  for 
any  reason.  Thorough  local  anesthesia  previous  to  the  injection  will 
probably  largely  prevent  it.  Infection  may  follow  the  introduction 
of  organisms  from  within  or  without.  Fagiuoli3  noted  the  develop- 
ment of  pleurisy  with  effusion  in  10  of  23  cases  in  which  he  had 
produced  artificial  pneumothorax.  It  has  been  estimated  that  an 
exudate  complicates  about  half  the  cases.  Weiss4  was  always  able 
to  demonstrate  tubercle  bacilli  in  the  effusion  by  animal  inoculation. 
Such  an  extension  of  the  tuberculous  process  cannot  be  regarded  as 
desirable. 

The  effect  of  maintaining  the  lung  in  a  collapsed  condition  for  a  long 
period  is  an  important  consideration.  In  collapse  of  the  lung  in  con- 
sequence of  pleurisy  with  effusion,  the  formation  of  extensive  pleural 
adhesions  and  of  dense  connective  tissue  on  the  surface  and  within 
the  substance  of  the  lung  may  develop  in  the  course  of  time  and  pre- 
vent reexpansion.  Such  indurative  changes  are  more  common  with 
empyema  than  with  serofibrinous  effusions  and  are  more  pronounced 
the  longer  the  lung  is  allowed  to  remain  in  a  contracted  and  atelectatic 
condition.  They  constitute  an  important  argument  for  the  early  re- 
moval of  inflammatory  and  especially  purulent  fluid.  Similar  changes 
in  the  pleura  and  lung  have  been  observed  as  a  complication  of  arti- 
ficial pneumothorax.  Graetz5  demonstrated  dense  fibrous  thickening 
of  the  pleura  over  the  collapsed  lung.  Weiss6  observed  such  changes 
in  the  pleura  in  two  cases  at  autopsy.  Bruns7  found  thickening  of 
the  pulmonary  pleura  and  an  increase  in  the  peribronchial  and  peri- 
vascular connective  tissue  after  experimental  pneumothorax  in  animals. 
Kaufmann's8  findings  are  still  further  confirmatory  and  suggest  great 

1  On  releasing  the  pressure,  the  nitrogen  ordinarily  fails  to  reenter  the  tubing  and 
the  proximal  branch  of  the  manometer  indicates  a  corresponding  elevation.  Immo- 
bility of  the  manometer  even  with  forced  breathing  suggests  that  the  nitrogen  has 
diffused  itself  into  the  tissues  or  penetrated  a  vessel,  while  respiratory  oscillations 
suggest  its  presence  in  a  closed  vesicle  or  between  the  layers  of  the  pleura?.  The  degree 
of  negative  pressure  and  the  amplitude  of  the  respiratory  oscillations  permit  of  a 
decision  between  its  entrance  into  a  closed  vesicle  and  the  pleural  sac.  If  the  latter 
is  the  case,  the  negative  pressure  and  the  oscillations  are  much  more  marked. 

2  Verhandlungen  des  Congresses  f.  innere  Med.,  1908,  vol.  xxv. 

3  Munch,  med.  Woch.,  May  7,  1912.  4  Beitr.  z.  Klinik  d.  Tub.,  1912,  xxiv,  333. 
6  Ibid.,  1908,  Bd.  x,  p.  249.                 6  Loc.  cit.,  p.  348.  7  Ibid.,  1909,  xii,  1. 

8  Ueber  die  Veranderung  d.  Pleura  u.  Lungen  gesunder  Hunde  mit  kiinstlichen  Pneu- 
mothorax, Ibid.,  1912,  Bd.  xxiii,  p.  57. 


584  DISEASES  OF   THE  PLEURA 

caution  in  the  adoption  of  the  method.  He  found  the  lung  incapable 
of  reexpansioE  in  consequence  of  such  changes.  Pulmonary  collapse 
is  likely  to  be  more  complete  in  those  parts  of  the  lung  which  are  little 
or  not  at  all  involved  arid  it  may  be  regarded  as  questionable  whether 
the  risk  of  materially  diminishing  or  even  abolishing  the  function  of 
sound  parts  can  be  safely  taken. 

Emphysema  of  greater  or  less  extent  is  common  after  the  Murphy- 
Brauer  incision  method  but  is  more  annoying  than  dangerous.  It 
was  observed  in  60  per  cent,  of  Robinson  and  Floyd's  cases.  It  is  less 
frequent  when  Forlanini's  puncture  method  is  used.  The  rapid  evacua- 
tion of  the  contents  of  tuberculous  cavities  under  compression  may 
lead  to  further  infection  in  near-by  or  remote  parts  of  the  lung.  Dys- 
pnea and  collapse  from  displacement  of  the  mediastinum  and  heart, 
pain  from  the  stretching  of  adhesions  and  gastric  symptoms  from  dis- 
placement downward  of  the  diaphragm  may  follow. 

It  is  difficult  to  understand  how  if  immobilization  of  one  lung  is 
of  value  in  checking  a  tuberculous  process,  overwork  is  good  for  the 
other,  and  the  arguments  in  its  favor  seem  invalid. 

Results. — Among  the  more  immediate  effects  are  diminution  of 
fever  and  disappearance  of  night  sweats.  This  is  ascribed  to  dimin- 
ished absorption  of  toxic  material.  The  amount  of  sputum  may  at 
first  increase,  with  later  diminution  in  the  cough  and  amount  of 
expectoration.  In  a  few  instances,  apparent  arrest  of  the  tuberculous 
process  has  been  secured  but  detailed  statements  concerning  the  late 
results  in  any  large  series  are  not  yet  published. 

Should  the  method  be  used?  Artificial  pneumothorax  as  a  means  of 
treatment  for  pulmonary  tuberculosis  is  not  theoretically  sound.  Bilat- 
eral infection  with  tubercle  bacilli  is  almost  constant  and  immobiliza- 
tion of  one  lung  must  of  necessity  impose  a  greater  amount  of  work  on 
the  other.  The  dangers  are  considerable  and  sufficient  to  discourage 
support  of  the  method,  unless  results  so  favorable  as  to  justify  the 
risks  can  be  demonstrated.  The  results  thus  far  are.  not  highly 
promising. 

Diagnosis. — When  in  the  course  of  chronic  pulmonary  tuberculosis 
there  is  sudden  pain  in  the  side,  immediately  followed  by  severe 
dyspnea,  pneumothorax  should  be  suspected.  Resonance  on  'per- 
cussion with  suppression  or  absence  of  the  respiratory  murmur  often 
gives  the  first  intimation  of  the  nature  of  the  trouble.  The  determina- 
tion of  displacement  of  the  heart  away  from  the  affected  side  is  con- 
firmatory and  the  diagnosis  may  be  regarded  as  established  if  the 
succussion  splash  of  pleural  fluid  is  heard.  Other  signs  of  importance 
are  diminished  or  absent  tactile  fremitus,  voice  sounds  and  whisper, 
the  amphoric  phenomena  (amphoric  breathing,  rales,  cough,  vocal 
resonance,  whisper,  and  heart  sounds),  metallic  tinkle,  coin-sound, 
and  movable  dulness  at  the  base  with  horizontal  upper  border  irres- 
pective of  the  position  of  the  patient.  The  auscultatory  phenomena 
are  essential  for  the  diagnosis.     With  mild  symptoms  and  a  small 


PNEUMOTHORAX  585 

pneumothorax,  especially  if  uncomplicated  by  fluid,  the  diagnosis  is 
difficult  and  the  condition  is  probably  frequently  overlooked.  Exami- 
nation by  means  of  the  x-rays  furnishes  valuable  data  and  may  make 
a  diagnosis  possible  when  other  means  fail. 

There  may  be  difficulty  in  differentiating  pneumothorax  from  the 
following  conditions: 

A  large  pulmonary  cavity,  in  common  with  pneumothorax,  may 
show  resonance  or  tympany  on  percussion,  cracked-pot  sound,  changes 
in  the  percussion  note  with  the  mouth  open  or  closed,  on  changing 
the  position  of  the  patient  and  during  inspiration  or  expiration.  If 
the  cavity  is  large  and  contains  thin  fluid,  there  may  be  movable 
dulness  with  horizontal  upper  border  below  the  resonant  area.  Am- 
phoric breathing,  metallic  tinkle,  the  coin-sound  and  succussion  splash 
may  also  be  present.  With  cavity,  however,  the  symptoms  are  likely 
to  be  gradually  progressive,  without  a  history  of  sudden  pain  and  severe 
dyspnea.  With  cavity  also  the  affected  side  is  likely  to  be  retracted  and 
the  intercostal  spaces  narrowed.  The  upper  lobes  or  the  apex  are  likely 
to  be  affected  over  a  less  extensive  and  more  definitely  circumscribed 
area  over  which  there  is  loud  bronchial  breathing,  increase  of  voice, 
whisper  and  tactile  fremitus  and  abundant  rales.  The  heart  is  drawn 
toward  the  affected  side  and  the  diaphragm  elevated  rather  than 
depressed.  In  cases  where  there  is  a  large  loss  of  pulmonary  sub- 
stance involving  the  greater  part  or  the  whole  of  one  lung  the  differ- 
entiation may  be  difficult.  Examination  by  means  of  the  a'-rays  may 
be  of  assistance.  The  absence  of  the  shadow  of  the  retracted  lung  at 
the  root  and  the  presence  of  a  shadow  with  a  central  clear  area  are 
suggestive  of  cavity. 

Subphrenic  pyopneumothorax,  first  accurately  described  by  Leyden1 
may  offer  great  difficulty.  A  collection  of  air  and  pus  is  present 
between  the  diaphragm  and  the  liver  or  between  the  diaphragm  and 
the  spleen,  stomach,  and  colon.  Perforation  of  a  gastric  or  duodenal 
ulcer  or  the  appendix  are  the  usual  causes,  but  in  rare  instances,  as 
in  the  case  reported  by  Umber,2  gas  may  be  formed  by  the  colon 
bacillus  and  without  evidence  of  perforation  of  the  intestine.  The 
right  or  left  side  may  be  affected  and  the  diaphragm  elevated  as  far  as 
the  third  or  even  the  second  rib  with  displacement  downward  of  the 
liver  and  other  abdominal  organs.  Over  the  cavity  containing  air 
and  fluid,  occupying  the  lower  part  of  the  chest,  there  are  the  physical 
signs  of  pyopneumothorax.  There  may  be  resonance  or  tympany  on 
percussion  above,  movable  dulness  below,  diminished  and  amphoric 
or  absent  respiratory  murmur,  vocal  and  tactile  fremitus  and  whisper 
and  metallic  tinkle,  coin-sound,  and  succussion  splash.  Absence  of 
cough  and  expectoration  and  a  history  of  preceding  abdominal  symp- 
toms may  suggest  an  abdominal  origin,  the  heart  is  only  slightly  dis- 
placed, the  intercostal  spaces  may  show  inspiratory  depression,  the 

1  Ztschr.  f.  klin.  Med.,  1880,  vol.  i,  and  Berl.  klin.  Woch.,  1892,  vol.  xlvi. 

2  Mitth.  a.  d.  Grenzgeb.  d.  Med.  u.  Chir.,  1900,  vol.  vi. 


586  DISEASES  OF   THE  PLEURA 

vesicular  hrc-at hinu  terminates  abruptly  where  the  signs  of  pyopneu- 
mothorax begin  and  respiratory  mobility  of  the  pulmonary  margin 

may  be  determined.  Foul  pus  with  a  fecal  odor  may  be  demonstrated 
by  exploratory  puncture  and  an  increase  in  the  tension  during  inspira- 
tion and  decrease  during  expiration,  as  suggested  by  Pi'nhl,  may  be 
determined.  Examination  with  the  x-rays  may  furnish  important 
evidence.  In  cases  in  which  the  pyopneumothorax  is  circum- 
scribed and  the  upward  dislocation  involves  only  a  part  of  the  dia- 
phragm, an  abrupt  dome-like  elevation  of  the  shadow  may  be  noted, 
with  evidence  of  air  above  and  fluid  below.  With  larger  accumula- 
tions the  diaphragm  may  be  elevated  as  a  whole  although  still  main- 
taining its  oval  contour  with  persistence  of  a  relatively  clear  space 
in  the  costophrenic  sinus.  If,  as  not  infrequently  happens,  pleurisy 
with  effusion  complicates  the  process,  the  x-ray  picture  is  obscured. 
On  examination  with  the  fluoroscope  inspiratory  depression  and 
expiratory  elevation  of  the  diaphragm  may  be  seen  and  the  diaphrag- 
matic excursion  is  usually  greater  than  with  pneumothorax. 

Diaphragmatic  hernia  may  closely  resemble  pneumohydrothorax. 
Lacher1  and  Grosser2  have  reviewed  the  reported  instances  which 
comprise  for  the  most  part  autopsy  cases.  The  diagnosis  is  seldom 
made  during  life  and  in  the  more  chronic  cases  has  been  established 
in  only  about  a  dozen  instances. 

True  diaphragmatic  hernia  may  in  rare  instances  be  congenital 
(the  much  discussed  eventratio  diaphragmatica  being  of  this  sort)  but 
is  more  commonly  acquired  as  the  result  of  stab  or  gun-shot  wounds, 
a  fall,  contusion  or  concussion.  The  left  side  is  usually  involved 
and  the  stomach  protrudes  into  the  chest.  With  a  large  defect  in 
the  diaphragm  the  transverse  colon,  the  omentum,  small  intestine, 
and  even  the  liver  or  spleen  may  be  contained  in  the  sac.  In  common 
with  pneumohydrothorax,  there  may  be  enlargement  of  the  side, 
diminished  respiratory  excursion,  diminished  amplitude  or  absence 
of  the  diaphragm  shadowy  immobility  of  the  pulmonary  margin  as 
determined  by  percussion,  dislocation  of  the  heart  and  mediastinum, 
tympany  on  percussion  above  with  dulness  shifting  with  change  of 
position  below,  coin-sound,  diminished  respiratory  murmur,  voice 
sounds  and  tactile  fremitus  and  succussion  splash.  On  examination 
with  the  x-rays,  an  area  suggesting  air  above  and  fluid  below  may  be 
seen,  and,  as  in  pneumohydrothorax,  the  fluid  may  be  seen  to  main- 
tain a  horizontal  upper  border  on  changing  the  position  of  the  patient. 
Waves  of  surface  motion  may  also  be  observed  during  respiration  and 
with  cardiac  systole. 

A  history  of  trauma,  such  gastro-intestinal  symptoms  as  pain, 
attacks  of  colic,  nausea,  and  vomiting  and,  in  rare  instances,  hemate- 
mesis  and  the  absence  of  cough  and  expectoration  may  call  attention  to 
the  abdomen  as  a  source  of  the  disturbance.    Changes  in  the  physical 

1  Deut,  Arch.  f.  klin.  Med.,  1880,  vol.  xxvii. 

2  Wien.  klin.  Woch.,  1899,  p.  655. 


PNEUMOTHORAX  587 

signs  dependent  on  a  full  or  empty  stomach,  sounds  over  the  chest 
resembling  the  movement  of  flatus  in  the  intestine  and  the  absence  of 
stomach  tympany  at  its  normal  position  after  inflation  with  gas  may 
serve  to  suggest  the  diagnosis.  The  x-ray  examination  may  show 
inspiratory  depression  and  expiratory  elevation  of  the  fluid  funlike 
the  paradoxical  mobility  in  pneumohydrothorax)  and  after  a  bismuth 
meal  the  position  and  outline  of  the  stomach  or  intestines  in  the  thorax. 

In  pneumonia  over  and  beside  the  consolidated  area  and  in  pleurisy 
with  effusion  over  the  collapsed  lung  the  percussion  note  may  have  a 
tympanitic  and  metallic  quality,  and  amphoric  auscultatory  phenom- 
ena may  be  present,  but  in  the  former  the  history  and  clinical  course 
and  in  both  the  increase  of  voice,  whisper,  and  tactile  fremitus  and  the 
absence  of  metallic  tinkle,  coin-sound  and  succussion  splash  and 
movable  dulness  with  horizontal  upper  border  usually  serve  to  make 
the  differentiation. 

Recognition  of  the  type  of  pneumothorax  is  not  always  easy  nor  is 
it  usually  of  practical  importance.  In  the  valvular  form  the  dyspnea 
is  likely  to  be  severe  and  persistent  or  gradually  increasing  with  dis- 
tention of  the  side  and  marked  dislocation  of  the  heart,  mediastinum, 
and  diaphragm.  Intrapleural  tension  is  likely  to  be  persistently 
positive.  With  open  pneumothorax,  the  dyspnea,  distention  of  the 
side,  and  dislocation  of  organs  is  less  marked.  Changes  in  the  per- 
cussion note  with -the  mouth  open  and  closed  are  more  likely  to  be 
present.  Intrapleural  tension  is  that  of  the  atmosphere  with  respira- 
tory oscillations  about  the  zero  point  and  there  is  a  rapid  return  to 
atmospheric  pressure  after  aspiration.  A  gas  analysis  which  shows 
5  per  cent,  or  less  of  C02  or  a  persistent  increase  in  0  in  successive 
portions  removed  suggests  an  open  fistula.  When  the  pneumothorax 
becomes  closed  the  dyspnea  diminishes,  displaced  organs  return,  posi- 
tive pressure  may  persist  at  the  height  of  inspiration  and  gas  analysis 
may  show  a  large  percentage  of  CO2.  The  determination  of  the  cause 
is  important.  A  history  of  preceding  hemoptysis  out  of  a  clear  sky 
or  a  primary  pleurisy,  cough  for  several  months,  night  sweats,  fever 
and  failing  weight  and  strength  usually  indicate  tuberculosis,  which 
owing  to  the  compression  of  the  lung  oftentimes  can  be  established  by 
the  finding  of  tubercle  bacilli  in  the  expectoration.  The  fact  that 
from  80  to  90  per  cent,  of  all  cases  are  of  tuberculous  origin  may 
well  influence  a  decision  in  doubtful  cases,  and  all  cases  should  be 
regarded  as  tuberculous  until  proved  otherwise. 

Course  and  Prognosis.— This  depends  for  the  most  part  on  the  under- 
lying disease.  The  pneumothorax  is  of  itself  usually  of  relatively 
little  importance,  as  the  patient  soon  develops  a  tolerance  of  the  con- 
dition. Air  alone  does  not  irritate  the  pleura  and  is  usually  absorbed 
in  the  course  of  from  one  to  two  months. 

As  a  complication  of  pulmonary  tuberculosis,  however,  it  intro- 
duces very  definite  dangers  and  hastens  the  fatal  termination.  The 
rupture  of  a  small  subpleural  tubercle,  a  tuberculous  cavity  or  a  pleural 


588  DISEASES  OF  THE  PLEURA 

adhesion  usually  leads  to  tuberculous  or  pyogenic  infection  of  the 
pleura,  with  the  formation  of  a  serofibrinous  or  purulent  effusion,  in 
consequence  of  which  the  fever  becomes  more  marked  and  emaciation 
progresses  more  rapidly.  West1  finds  the  mortality  highest  in  the 
first  few  days,  10  of  .'!!)  cases  dying  on  the  first  day,  IS  during 
the  first  week.  Among  74  cases,  45  died  in  the  first  month.  The 
general  mortality  was  about  70  per  cent.  Among  Drasche's  198  cases, 
71  per  cent,  died  within  the  first  fourteen  days.  Death  may  be  as- 
cribed to  suffocation  from  the  pneumothorax  itself  or  flooding  of  the 
opposite  lung  with  pus,  to  rapid  extension  of  tuberculous  or  septic 
material  into  the  pleura  or  to  the  original  disease,  phthisis.  Hughes'2 
remarkable  patient  lived  at  least  three  years  and  two  months 
after  the  occurrence  of  pneumothorax,  was  able  to  attend  his  regular 
business  and  amused  his  friends  by  the  succussion  sound.  In  a  small 
proportion  of  the  cases  an  effusion  fails  to  develop,  or  if  present  is 
absorbed  or  successfully  evacuated  and  the  patient's  recovery  is  per- 
manent and  complete. 

Spengler3  has  reported  10  cases  of  tuberculous  pneumothorax 
with  recovery  and  in  6  there  was  simultaneous  arrest  of  the  pulmonary 
tuberculosis,  but  his  experience  has  been  very  unusual  and  contrary 
to  that  of  most  observers.  To  the  time  of  his  report  a  total  of  38  cases 
of  healed  tuberculous  pneumothorax  could  be  found  in  the  literature. 
The  favorable  outcome  in  these  cases  has  been  used  as  an  argument 
in  favor  of  artificial  pneumothorax  in  the  treatment  of  pulmonary 
tuberculosis,  but  it  must  be  remembered  that  recovered  cases  com- 
prise only  a  small  proportion  of  the  total  number.  West  estimates 
complete  recovery  at  not  over  10  per  cent,  and  this  may  be  regarded 
as  a  conservative  estimate. 

The  prognosis  of  the  spontaneous  cases,  unless  of  the  suffocative 
type,  is  favorable,  only  one  death  occurring  in  58  cases  studied  by 
Fussell  and  Riesman.  Uncomplicated  traumatic  cases  usually  also 
do  well.  Suffocative  pneumothorax  is  rapidly  fatal  unless  relieved  by 
operation. 

Treatment. — The  indications  are,  on  the  one  hand,  to  promote 
closure  of  the  pulmonary  fistula  and  prevent  infection  of  the  pleura 
and  on  the  other  to  relieve  a  dangerous  degree  of  embarrassment  to 
respiration  and  the  unfavorable  consequences  of  pleural  effusion  more 
especially  of  the  purulent  form.  Inasmuch  as  removal  of  air  or  fluid 
by  decreasing  intrapleural  tension  tends  to  reinflate  the  collapsed 
lung,  reopen  a  pulmonary  fistula  and  aspirate  infectious  material  from 
the  lung  or  bronchi  into  the  pleura  the  indications  are  mutually  con- 
flicting and  a  conservative  middle  course  is  often  the  wisest  plan. 

In  ordinary  and  other  than  urgent  cases  immediately  following  the 
rupture  the  patient  should  be  absolutely  at  rest  in  bed.  Irritative 
and  unproductive  cough  should  so  far  as  possible  be  suppressed  and 

1  Lancet,  1897,  i,  1264.  2  Guy's  Hosp.  Rep.,  2d  S.,  vol.  viii. 

3  Beitr.  z.  klin.  Chir.,  1906,  xliv,  68. 


PNEUMOTHORAX  589 

deep  respiration  avoided  in  order  to  hasten  closure  of  the  fistula  and 
prevent  further  entrance  of  air  into  the  pleura.  Strapping  the  affected 
side  with  adhesive  plaster  may  help  and  morphin  may  be  of  assistance 
in  quieting  cough.  In  mild  and  moderately  severe  cases  no  further 
treatment  is  usually  needed.  The  patient  should  be  absolutely  quiet 
for  two  or  three  weeks  or  until  there  is  reason  to  believe  that  the  fistula 
is  closed.  Traumatic  and  spontaneous  cases  usually  do  well  under 
such  conservative  management. 

In  cases  in  which  the  pneumothorax  rapidly  increases,  with  urgent 
dyspnea,  cyanosis  and  great  displacement  of  the  heart,  immediate 
relief  must  be  offered.  Pneumothorax  acutissimus  and  certain  cases 
of  the  valvular  form  are  of  this  type.  Puncture  may  prove  life-saving. 
Aspiration  should  be  avoided  for  fear  of  reopening  the  fistula.  With 
valvular  pneumothorax  the  pleural  sac  is  likely  to  be  reinflated  and 
the  puncture  may  need  to  be  repeated  or  the  cannula  left  in  place 
for  a  time.  Infection  through  the  chest  wall  is  to  be  avoided  by  the 
strictest  asepsis.  Thoracotomy  with  insertion  of  a  drainage  tube, 
converting  the  valvular  into  open  pneumothorax  with  external  fistula, 
is  occasionally  necessary. 

With  hemopneumothorax  and  hydropneumothorax  with  a  small 
or  moderate  amount  of  fluid  and  without  pressure  symptoms,  it  is 
best  to  leave  the  fluid  undisturbed  for  at  least  two  or  three  weeks  or 
until  closure  of  the  fistula  is  established.  With  large  fluid  accumula- 
tions or  those  with  pressure  symptoms  it  may  be  necessary  to  tap, 
but  it  is  best  to  withdraw  only  small  amounts  at  frequent  intervals  and 
without  forcible  aspiration.  The  indications  are  essentially  those 
with  uncomplicated  serofibrinous  effusions  with  the  exception  that 
here  the  danger  incident  to  the  fluid  must  be  weighed  against  that  of 
opening  the  fistula,  and  the  latter  justifies  a  delay  in  doubtful  cases. 

Spengler  regards  an  exudate  as  desirable  to  promote  closure  of  the 
fistula,  further  compression  of  the  lung  and  arrest  of  the  tuberculous 
process,  and  would  allow  the  patient  to  be  up  and  about  as  soon  as 
possible  to  deepen  respiratory  motion  and  induce  pleural  infection. 
Such  an  extension  of  tuberculous  or  pyogenic  infection  to  the  pleura 
seems  to  me  undesirable  and  to  lead  to  more  rapid  progress  of  the 
disease. 

With  seropurulent  and  sterile  purulent  effusions  in  which  symptoms 
of  sepsis  are  absent  or  slight,  it  is  best  if  possible  to  wait  until  the 
fistula  is  closed.  If  removal  is  indicated  simple  aspiration  and  the 
repeated  removal  of  from  500  to  700  c.c.  may  suffice.  With  frankly 
purulent  fluid  containing  pyogenic  organisms  and  with  marked  symp- 
toms of  sepsis,  further  regard  for  the  fistula  must  be  abandoned  and 
free  drainage  established  as  for  ordinary  empyema.  With  putrid 
exudates  an  immediate  operation  is  demanded. 


INDEX. 


Abortive  pneumonia,  196 
Abscess,  in  Friedlander's  bacillus  pneu- 
monia, 238 
hemoptysis  in,  353 
pulmonary,  290 

after-treatment  of,  317 
bronchopneumonia  and,  291 
complications  of,  302 
condition  of  pleura  in,  296 
diagnosis  of,  303 
elastic  tissue  in,  299 
embolic  form  of,  292 
etiology  of,  290 
exploratory  puncture  in,  308 
lobar  pneumonia  and,  290 
mortality  in,  310 
number  of  lesions  in,  295 
origin  of,  292 
pathology  of,  293 
physical  signs  of,  301 
pulmonary  induration  in,  296 
site  of  lesions  in,  295 
special  causes  of,  293 
sputum  in,  298 
symptoms  of,  297 
trauma  and,  292 
treatment  of,  311 

artificial  pneumothorax  in, 

317 
medical,  311 

pressure  apparatus  in,  317 
surgical,  311 

accidents  in,   315 
dangers  in,  315 
indications  for,  312 
pleurotomy  in,  314 
pneumectomy  in,  315 
pneumotomy  in,  314 
results  of  operation  in, 

316 
thoracotomy  in,  313 
a>ray  examination  in,  307 
subdiaphragmatic,  496 
Actinomyces,  atypical,  389 
bovis,  371 
colonies  of,  375 
granule,  372 

crushed,  372 
mode  of  infection  by,  376 
sugar-agar    suspension    cultures  of, 
374 


Actinomycosis,  371 
diagnosis  of,  384 
etiology  of,  371 
hemoptysis  in,  355 
of  omentum,  377 
pathogenesis  of,  378 
pathology  of,  379 
physical  signs  of,  381 
of  pleura,  533 
prognosis  of,  385 
prophylaxis  of,  385 
pulmonary,  primary,  378 

secondary,  378 
symptoms  of,  381 
treatment  of,  386 
Air  embolism,  345 
Albuminous  expectoration,  323,  515 
Alcoholics,  pneumonia  in,  196 
Amphoric  phenomena  in  pneumothorax, 

573 
Anaphylaxis,  bronchial  asthma  and,  48 
Anesthesia,  insufflation,  317 

local,  for  exploratory  puncture,  498 
Aneurysm,  aortic,  bronchostenosis  and, 
17 
hemoptysis  in,  353 
bronchiectasis  and,  110 
Animal  parasites,  404 
Anthracosis,  284 

spontaneous  pulmonary,  in  animals, 
278 
Anthrax,  tracheobronchitis  and,  83 
Antipneumococcus  serum,  172 
Antitoxin,  use  of,  in  asthma,  63 
Apical  pneumonia,  195 
Arteriosclerosis,  pulmonary,  451 
appearance  of,  451 
clinical  features  of,  452 
forms  of,  451 
Arthritis  in  lobar  pneumonia,  215 
Ascaris,  426 

Aspergillosis  in  animals,  400 
in  man,  401 
pulmonary,  399 

diagnosis  of,  402 
etiology  of,  399 
hemoptysis  in,  355 
pathology  of,  401 
prognosis  of,  402 
prophylaxis  of,  403 
symptoms  of,  402 
treatment  of,  403 
Aspergillus  fumigatus,  399 


592 


INDEX 


Aspiration  of  pleural  (luids,  510 

pneumonia,  bronchopneumonia  and, 

247 
Asthenic  pneumonia,  194 
Asthma, -bronchial,   44.     See  Bronchial 

asthma.  , 

bronchostenosis  and,  18 

cardiac.  108,  321 

chronic  bronchitis  and,  96 

renal,  60 
Atelectasis,  129 

acquired,  130, 136 

treatment  of,  138 

bronchial  occlusion  in,  131 

bronchitis,  acute,  and,  90 

bronchopneumonia  and,  133,  250 

in  bronchostenosis,  18 

classification  in,  129 

collapse  induration  in,  136 

compression,  130 

congenital,  130, 135 
treatment  of,  138 

diagnosis  of,  138 

dyspnea  in,  137 

effect  of,  on  circulation,  134 

etiology  of,  130 

history  of,  129 

lrypostatic  pneumonia  in,  133 

inflammatory  processes  in,  137 

medicolegal  aspect  in,  134 

obstruction,  130 

pathogenesis  of,  130 

pathology  of,  132 

physical  signs  in,  135 

prognosis  of,  138 

pulmonary  collapse  in,  137 

retraction,  130 

symptoms  of,  135 

treatment  of,  138 

z-ray  examination  in,  137 
Atelectatic  bronchiectasis,  127, 133 
Autoserotherapy  in  treatment  of  sero- 
fibrinous pleuritis,  518 


B 


Bacelli's  sign,  485,  521 

Bacillus  pneumoniae,  Friedlander's,  234 

Bacteria,  dust  and,  282 

"Black  death,"  257 

"spit,"  284 
Blastomycetes  in  lung,  395 
Blastomycosis,  bronchial,  128 

prognosis  in,  128 

recovery  in,  128 

sputum  in,  128 

symptoms  in,  128 
pulmonary,  392 

cutaneous  lesions  in,  396 

diagnosis  of,  397 

etiology  of,  392 

immunity  in,  394 

microorganisms  of,  392 
cultures  of,  393 


Blastomycosis,    pulmonary,     pathology 

of,  395 
prognosis  of,  398 
symptoms  of,  397 
treatment  of,  398 
Blood  in  lobar  pneumonia,  204 
Bordet-Gengou  bacillus,  81 
Bothriocephalus  latus,  422 
Bronchi,  carcinoma  of,  22 
dilatation  of,  108 
diseases  of,  17 
enchondromas  in,  22 
foreign  bodies  in,  29 

diagnosis  of,  34 
etiology  of,  30 
pathology  of,  30 
prognosis  of,  35 
signs  of,  32 
symptoms  of,  31 
treatment  in,  36 
x-ray  examination  in,  32 
large  and  medium-sized,  stenosis  of, 

17 
lesions  of,  hemoptysis  in,  354 
lipoma  in,  22 
papilloma  in,  22 
polypi  in,  22 
scleroma  of,  28 

smaller,  bronchostenosis  and,  18 
syphilis  of,  23 
tuberculosis  of,  27 
tumors  of,  22,  427,  428 
Bronchial  asthma,  44 
age  in,  50 

anaphylaxis  and,  48 
attack  in,  52 

paroxysm  in,  53 
treatment  of,  60 
auscultation  in,  53 
bronchostenosis  and,  18 
Charcot-Leyden     crystals     in, 

55 
complications  of,  58 
course  of,  58 

Curschmann's  spirals  in,  53 
diagnosis  of,  58 
drugs  in,  46,  61,  63 
eosinophiles  in,  57 
etiology  of,  49 

exciting,  51 
heredity  in,  49 
Laennec's  perles  in,  53 
Meltzer's  theory  in,  49 
nervous  system  in,  48 
nose  and,  50 
pathology  of,  51 
percussion  in,  53 
physical  signs  in,  53 
predisposing  factors  in,  49 
prevention    of    recurrences    in 

treatment  of,  62 
prognosis  of,  60 
sex  in,  50 

spasm  of  diaphragm  in,  48 
sputum  in,  53 


INDEX 


593 


Bronchial  asthma,  swelling  of  bronchial 
mucous  membranes  in,  46 
symptoms  of,  52 
treatment  of,  60 
climate  in,  64 
danger     of      anaphylactic 

shock  in,  63 
general,  62 

removal  of  cause  in,  62 
blastomycosis,  128 
"  colic,"  41 

theory  in  bronchiectasis,  114 
wall,    diseases    of,    bronchostenosis 
and,  17 
Bronchiectasis,  108 

acute  infection  and,  109 
aneurysm  and,  110 
atelectatic,  127 
bacteriology  of,  110 
bronchial  theory  in,  114 

tumor  and,  110 
bronchopneumonia  and,  252 
bronchopulmonary  form  of,  117 

theory  in,  114 
bronchostenosis  and,  110 
cardiac  hypertrophy  in,  114 
cerebral  abscess  in,  114 
chronic   interstitial   pneumonia   in, 

113 
clinical  antecedents  of,  109 
complications  of,  118 
congenital,  126 
cough  in,  116 
diagnosis  of,  120 
differentiation  of,  112 
empyema  and,  121 
endocarditis  in,  114 
etiology  of,  108 
exploratory  puncture  in,  122 
fetal,  126 

hemoptysis  in,  116,  353 
hyperplasia  in,  113 
hypertrophic       pulmonary      osteo 

arthropathy  and,  118 
incidence  of,  108 
mediastinal  tumor  and,  110 
meningitis  in,  114 
pain  in,  116 
pathology  of,  110 
pericarditis  in,  114 
physical  signs  in,  116 
pleuritis  in,  113 
prognosis  of,  122 
prophylaxis  of,  122 
pulmonary  disease  and,  109 

theory  in,  114 
pure,  117 
sex  and,  109 
sputum  in,  116 
symptoms  of,  115 
syphilitic  stenosis  and,  122 
telangiectatic,  126 
theories  of,  114 
treatment  of,  123 

artificial  pneumothorax  in,  126 
38 


Bronchiectasis,    treatment    of,    general, 
123 

inhalations  in,  123 

internal  medication  in,  124 

intratracheal  inj  ctions  in,  124 

postural,  124 

special,  123 

surgery  in,  125 
tuberculosis  and,  121 
universal,  126 
rc-ray  examination  in,  122 
Bronchiolitis  exudativa,  47 

obliterans,  bronchostenosis  and,  18 
Bronchitis,     77 

bacteriology  of  sputum  in,  85 
capillary,  94 

bronchostenosis  and,  18 
chronic,  94 

age  in,  97 

asthma  and,  96 

bronchial  disease  and,  96 

bronchostenosis  and,  96 

circulatory  system  in  etiology 
of,  94 

clinical  varieties  of,  100 

complications  of,  103 

cough  and,  99 

diagnosis  of,  130 

examination    of   blood   in, 
104 
of  sputum  in,  104 

dyspnea  and,  99 

emphysema  and,  96,  103 

etiology  of,  94 

pathology  of,  98 

prognosis  of,  104 

pulmonary  diseases  and,  95 

sex  in,  97 

symptoms  of,  98 

syphilis  and,  96 

treatment  of,  105 
hygienic,  106 

internal  medication  in,  107 
local,  106 
posture  in,  106 

tuberculosis  and,  95 
diseases  of  nasopharynx  and,  97 

of  tonsils  and,  97 
e'osinophile,  101 
fibrinosa,  65 

bronchial  asthma  and,  66 

bronchostenosis  and,  18 

classification  of,  65 

cough  in,  69 

cyanosis  in,  69 

diagnosis  of,  72 

dyspnea  in,  69 

etiology  of,  65 

expectoration  of  casts  in,  67,  71 

hemoptysis  in,  70 

hoarseness  in,  69 

occurrence  of,  65 

pathology  of,  68 

physical  examination  in,  70 

prognosis  of,  72 


594 


INDEX 


Bronchitis,  fibrinosa,  symptoms  of,  69 

treat  oaeni  of,  72 
in  lobar  pneumonia,  205 
mucopurulent,;  101 
obliterans,  7  I 

diagnosis  of,  75 

el  iology  of,  74 

pathology  of,  7  1 

prognosis  of,  76 

prophylaxis  of,  76 

symptoms  of,  75 

treatment  of,  7(5 
purulent,  101 
putrid,  102 
Bronchooldiosis,  128 
Bronchopneumonia,  218,  245 

acute,  complicating  cases  in,  246 

aspiration  pneumonia  and,  247 

atelectasis  and,  133,  249 

bacteriology  of,  248 

bronchostenosis  and,  18 

in  children,  256 

complications  of,  255 

cylindrical  bronchiectasis  and,  252 

debilitating  conditions  and,  247 

diagnosis  of,  259 

emphysema  in,  250 

etiology  of,  245 

experimental,  249 

frequency  of,  245 

history  of,  245 

measles  and,  257 

microscopic  examination  in,  251 

mixed  infection  in,  251 

pathology  of,  249 

physical  signs  of,  254 

primary  acute,  246 

prognosis  of,  261 

prophylaxis  of,  261 

pulmonary    abscess    and    gangrene 

and,  291 
results  of,  251 
secondary,  246 
sequelae  of,  255 
symptoms  of,  253 
treatment  of,  262 
tuberculous,  252 
types  of,  256 
whooping  cough  and,  257 
Bronchopulmonary   form    of   bronchiec- 
tasis, 117 
theory  in  bronchiectasis,  114 
Bronchorrhea  serosa,  102 
Bronchoscopy  in  bronchostenosis,  37 
Bronchostenosis,  17 

aortic  aneurysm  and,  17 
atelectasis  in,  18 
bronchial  asthma  and,  18 
bronchiectasis  and,  110 
bronchiolitis  obliterans  and,  18 
bronchitis  fibrinosa  and,  18 
bronchopneumonia  and,  18 
bronchoscopy  in,  37 
bronchotomy  in,  38 
capillary  bronchitis  and,  18 


Bronchostenosis,  chronic  bronchitis  and, 
96 
cornage  in,  '_'(> 

diagnosis  of,  20 

tracheal  tug  in,  21 
./•-rays  in,  21 
dilatation  of  left  auricle  and,  17 
diseases  of  bronchial  wall  and,  17 
dyspnea  in,  19 
etiology  of,  17 

extrabronchial,  17 

intrabronchial,  18 

foreign  bodies  and,  18 

arising  from  within   in,   39 
diagnosis  of,  42 
etiology  of,  39 
pathology  of,  39 
prognosis  of,  43 
signs  of,  40 
symptoms  of,  40 
treatment  of,  43 
hoarseness  in,  19 
incrustation  of  tissue  and,  39 
mucus  and,  18 
pathology  of,  18 
petrification  of  bronchi  and,  39 
pneumobronchotomy  in,  39 
pneumohydrothorax  and,  17 
prognosis  of,  21 

pulmonary  tuberculosis  and,  18 
scleroma  and,  17 
signs  of,  19 

smaller  bronchi  and,  18 
stridor  in,  20 
suffocation  in,  19 
symptoms  of,  19 
irritative,  19 
syphilis  and,  17 
tracheotomy  in,  38 
treatment  of,  21 
tuberculosis  and,  17 
tumors  and,  17 
unilateral,  20 
Bronchotomy  in  bronchostenosis,  38 
Bronchus,  carcinoma  of,  430 
Byssinosis,  285 


Capillary  bronchitis,  245.  See  Broncho- 
pneumonia. 
Carcinoma  of  bronchi,  22 

with    metastasis     into    lymph 
gland,  430 
of  lung,  primary,  428 

etiology  of,  428 
incidence  of,  428 
pathology  of,  429 
of  pleura,  551 
Carcinosis,  miliary,  432 
Cardiac  hypertrophy    in  bronchiectasis, 

114 
Cardiovascular   system   in   lobar   pneu- 
monia, 207 


INDEX 


595 


Casts,    bronchial,    fibrinous    bronchitis 
and,  68,  70 

Catarrh,  dry,  100 

serous  form  of,  102 

Cell  emboli,  350 

Central  pneumonia,  194 

Cercomonas,  426 

Cerebral  abscess  in  bronchiectasis,  114 

Chalicosis,  284 

Charcot-Leyden    crystals    in    bronchial 
asthma,  47,  55 
in  other  conditions,  56 
in  pulmonary  distomatosis,  423 

Children,  pneumonia  in,  195 

Chyliform  pleural  fluids,  546 

Chylothorax,  546 

Chylous  pleural  fluids,  546 

Circulation,  effect  of  atelectasis  on,  134 

Circulatory  disturbances,  318 

Cirrhosis  of  lung,  264 

Cladothrix,  389 

Coagulation  time  in  lobar    pneumonia, 
205 

Coal  dust,  284 

Coin  sound  in  pneumothorax,  575 

Collapse  induration  in  atelectasis,  136 

Complement-fixation  test  in  diagnosis  of 
echinococcus  disease,  414 

Compression  atelectasis,  130 

Congenital  bronchiectasis,  126 

Congestion,    chronic     passive,     hemop- 
tysis in,  353 
of  lungs,  active,  319 
hypostatic,  321 
passive,  319 

"Cornage,"  20,  436 

Costatectomy    in    treatment    of    acute 
purulent  pleuritis,  527 
of  bronchiectasis,  126 
of      echinococcus     disease     of 
pleura,  562 

Costopneumopexy,  314 

Curschmann's  spirals,  48,  53 

Cysticercus  cellulosse,  426 

Cytodiagnosis,  500 

Cytology  of  pleural  effusions,  473,  554 


Diabetes,  pneumonia  and,  197 
Diaphragm,     spasm     of,    in     bronchial 

asthma,  48 
Diaphragmatic  pleurisy,  531 
Diphtheria,  bronchopneumonia  and,  257 

tracheobronchitis  and,  83 
Diphtheroid  bacilli  in  tracheobronchitis, 

81 
Distoma,  hepatic,  426 

pulmonary,  421 
Distomatosis,  pulmonary,  420 
complications  of,  424 
diagnosis  of,  425 
parasite  in,  420 
pathology  of,  422 


Distomatosis,   pulmonary,   prognosis  of, 
■125 
prophylaxis  of,  425 
symptoms  of,  423 
treatment  of,  425 
Dittrich's  plugs  in  gangrene,  301 
in  putrid  bronchitis,  102 
Drugs  in  bronchial  asthma,  46 
"Dry  pleurisy,"  535 
Dust,  bacteria  and,  282 
kinds  of,  284 
metastases,  282 
pulmonary  disease  and,  JJZ9 
Dyspnea  in  atelectasis,  137 
in  bronchostenosis,  19 


E 


Echinococcus  disease  of  the  lung,  404 
blood  in,  412 
cysts  in,  intact,  418 

ruptured,  419 
diagnosis  of,  412 

serum,  414 
duration  of,  412 
etiology  of,  404 
incidence  of,  404 
pathogenesis  of,  404 
pathology  of,  406 
primary,  404 
prognosis  of,  418 
secondary,  405 

by  extension,  405 
by  metastasis,  405 
signs  of,  407 

sources  of  infection  of,  404 
symptoms  of,  407 
thoracentesis  in,  415 
treatment  of,  418 
.x-ray  examination  in,  413 
of  pleura,  557 
primary,  557 
secondary,  558 
double,  414 
hooklets,  411 
parapleural,  558 
blood  in,  560 
diagnosis  of,  560 
prognosis  of,  562 
symptoms  of,  559 
treatment  of,  562 
parapulmonary,  406 

cysts  in,  intact,  406 
perforated,  406 
pulmonary,  404 
scolices,  410 
Edema,  pulmonary,  321 
acute,  322 

arteriosclerosis  in,  322 
cardiac  disease  in,  322 
doubtful  causes  of,  323 
infectious  disease  in,  322 
paracentesis  of  thorax  and 
abdomen  in,  323 


596 


INDEX 


Edema,  pulmonary,  acute,  renal  disease 
in,  322 
chronic,  322 
diagnosis  of,  325 
pathogenesis  of,  323 
pathology  of,  324 
progn6sis  of,  326 
symptoms  of,  324 
treatment  of,  326 
Elastic  tissue,  299 

in  chronic  bronchitis,  96 
Emboli,  cell,  350 
Embolism,  air,  345 
fat,  345 
hydatid,  351 
mercury,  348 
pulmonary,  328 
course  of,  336 
diagnosis  of,  341 
prognosis  of,  343 
symptoms  of,  336 
treatment  of,  343 
Emphysema,  140 

acute  vesicular,  140,  152 
causes  of,  152 
prognosis  of,  152 
atrophic,  153 

in  bronchopneumonia,  250 
chronic  bronchitis  and,  96,  103 
classification  of,  140 
collateral,  152 
compensatory,  140,  152 

lungs  in,  152 
complementary,  152 
diffuse  vesicular,  140 
age  and,  141 

alveolar  dilatation  in,  145 
bronchial  asthma  and,  140 
chronic  bronchitis  and,  140, 

146 
coalescence  of  cavities  in, 

145 
compression  of  the  trachea 

and,  140 
definition  of,  140 
diagnosis  of,  149 
etiology  of,  140 
examination      of,      micro- 
scopic, 145 
special     methods     of, 
148 
heart  in,  146 

examination  of,  148 
inheritance  in,  141 
mechanical  factors  in,  141 
nutritive   disturbances   in, 

141 
obstruction  of  air  passages 

and,  140 
occupation  and,  140 
pathogenesis  of,  141 
pathology  of,  144 
physical  signs  in,  147 
prognosis  of,  149 
sex  and,  141 


Emphysema,    diffuse    vesicular,    symp- 
toms in,  146 

treatment  of,  149 
whooping  cough  and,  1-10 
hypertrophic,  140 
idiopathic,  140 
interlobular,  153 
interstitial,  140,  153 
causes  of,  154 
lungs  in,  154 
occurrence  of,  153 
symptoms  of,  154 
large-lunged,  140 
mediastinal,  154 
causes  of,  154 
prognosis  of,  156 
symptoms  of,  155 
ordinary,  140 
partial,  152 
senile,  140,  153 
substantive,  140 
true,  140 
vicarious,  152 
Empyema,  bronchiectasis  and,  121 
encysted,  531 

diagnosis  of,  533 
encapsulation  of  pus  in,  532 
interlobar  empyema  in,  532 
sacculation  between    lung    and 

chest  wall  in,  532 
treatment  of,  533 
necessitatis,  523 
pulsating,  acute  purulent  pleuritis 

and,  521 
tuberculous,  in  acute  purulent  pleu- 
ritis, 528_ 
Enchondromas  in  bronchi,  22 
Encysted  empyema,  531 
Endocarditis  in  bronchiectasis,  114 

in  lobar  pneumonia,  207 
Endomyces,  392 

Endothelial  plaques  and  cells,  502 
Endothelioma  of  pleura,  551 
Eosinophile  in  bronchial  asthma,  57 
bronchitis,  101 
in  echinococcus  disease,  412 
in  hemorrhagic  pleural  fluid,  540 
in  traumatic  hemothorax,  542 
Erysipelas,  tracheobronchitis  and,  83 
Ether-pneumonia,  196 
Ethyl  hydrocuprein  in  treatment  of  pneu- 
monia, 224 


Fasciola  hepatica,  422 
Fat  embolism,  346 

prognosis  of,  348 

symptoms  of,  348 
Fetal  bronchiectasis,  126 
"Fettkornchenkugeln,"  439 
Friedlander's  bacillus,  cultures  of,  235 

etiology  of,  234 

infection  by,  complications  in, 
239 


INDEX 


597 


Friedlander's     bacillus,     infection     by, 
diagnosis  of,  239 
prognosis  of,  240 
symptoms  in,  239 
treatment  of,  240 

occurrence  of,  234 

pathology  of,  238 

pneumoniae,  234 

in  pulmonary  exudate,  236 

relation  to  pneumonia  of,  235 

in  sputum,  236 


G 


Gangrene,  hemoptysis  in,  353 
pulmonary,  290 

after-treatment  of,  317 
bronchopneumonia  and,  291 
complications  of,  302 
condition  of  pleura  in,  296 
diagnosis  of,  303 
embolic  form  of,  292 
etiology  of,  290 
exploratory  puncture  in,  308 
lobar  pneumonia  and,  290 
mortality  in,  310 
number  of  lesions  in,  395 
origin  of,  292 
pathology  of,  293 
physical  signs  of,  301 
progress  of,  308 
pulmonary       induration       in, 
296 
infections  and,  290 
site  of  lesions  in,  295 
special  causes  of,  293 
symptoms  of,  301 
trauma  of,  292 
treatment  of,  311 

artificial  pneumothorax  in, 

317 
medical,  311 
pressure      apparatus      in, 

317 
surgical,   311 

accidents  in,  315 
dangers  in,  315 
indications  for,  312 
pleurotomy  in,  314 
pneumectomy  in,  315 
pneumotomy  in,  314 
results  of  operation  in 

316 
thoracotomy  in,  313 
x-ray  examination  in,  307 
"  Ganister  disease,"  284 
Gastro-intestinal  system  in  lobar  pneu- 
monia, 210 
Glanders,  tracheobronchitis  and,  83 
"  Grinder's  asthma,"  284 

rot,"  284 
Grocco's  triangle,  488 
Gummata  in    hereditary    form    of    pul- 
monary syphilis,  364 


H 


Hemohydrothorax,  540 
Hemopneumothorax,  543 
Hemoptysis,  352 
in  abscess,  353 
in  actinomycosis,  355 
from  animal  parasites,  355 
in  aortic  aneurysm,  353 
in  bronchiectasis,  116,  353 
in  chronic  passive  congestion,  353 
in  constitutional  diseases,  355 
diagnosis  of,  355 
etiology  of,  352 
in  gangrene,  353 
in  leprosy,  355 
in  lesions  of  bronchi,  354 

of  trachea,  354 
in  lung  hernia,  449 
in  mechanical  injuries,  354 
in  new  growths,  354 
parasitic,  420 
in  pneumonia,  352 
in  pulmonary  aspergillosis,  355 
infarction,  353 
tuberculosis,  352,  357 

febrile  reaction  in,  359 
pathology  of,  358 
prognosis  of,  360 
symptoms  of,  358 
treatment  of,  361 
drugs  in,  362 
limitation    of    motion 

in,  363 
venesection  in,  363 
toxic  causes  of,  355 
Hemorrhagic  pleural  fluids,  539 
Hemoserothorax,  539 
primary,  539 
secondary,  540 
traumatic,  541 

complications  of,  543 
diagnosis  of,  543 
etiology  of,  541 
prognosis  of,  544 
sequelae  of,  543 
special  pathology  of,  541 
symptoms  of,  542 
treatment  of,  544 
Hepatic  distoma,  426 
Hernia  of  lung,  448 
"  Herzfehlerzellen"  in  sputum,  319 
"Hippocratic  succussion,"  564 
Hydatid  embolism,  351 
Hydrothorax,  537 

cardiac  insufficiency  and,  537 
renal  disease  and,  537 
symptoms  of,  538 
treatment  of,  538 
Hyperplasia  in  bronchiectasis,  113 
Hypertrophic       "pulmonary"       osteo- 
arthropathy,      bronchiectasis       and, 
118 
Hypostatic  congestion  of  lungs,  321 
pneumonia,  321 


598 


TNDEX 


Incision,  exploratory,  for  empyema,  52G 
Infarct  ion,  pulmonary,  332 
appearance  of,  334 
course  of ,  338 
diagnosis  of,  342 
hemoptysis  in,  353 
relation     to     thrombosis     and 

embolism,  333 
symptoms  of,  338 
treat  incut  of,  344 
Infectious  pleuritis,  469 
Influenza,  acute   tracheobronchitis   and, 
78 
bacillus,  bronchiectasis  and,  110 
pandemic,  79 
Inoscopy,  468,  504 
Insanity,  pneumonia  and,  199 
Insufflation,  intratracheal,  317 
lodophilia  in  lobar  pneumonia,  205 


Jaundice  in  lobar  pneumonia,  210 


Kronig's  method  in  treatment  of  acute 
serofibrinous  pleuritis,  510 


Laennec's  perles  in  bronchial  asthma, 

53 
Laryngeal  stenosis,  symptoms  of,  20 
Leprosy,  hemoptysis  in,  355 
Lipoma  in  bronchi,  22 
of  the  pleura,  550 
Lithosis,  284 

Litten's  phenomenon,  481 
Lobar  pneumonia,  157.    See  Pneumonia, 

lobar. 
Lung,  cancer  of,  primary,  428 
congestion  of,  active,  319 

passive,  319 
diseases  of,  129 
hernia,  448 

acquired,  448 
congenital,  448 
hemoptysis  in,  449 
pain  in,  449 
size  of,  449 
treatment  of,  450 
voice  in,  449 
induration  of,  brown,  319 
sarcoma  of,  primary,  432 
tumors  of,  427 
benign,  427 
malignant,  428 
Lung-fluke    disease.     See   Distomatosis 

pulmonary,  420. 
Lymphocytosis,  501 


M 


Malaria,  pneumonia  and,  199 

tracheobronchitis  and,  S3 
Marie's  disease,  118 
Massive  pneumonia,  1'.)  1 
Measles,  bronchopneumonia  and,  257 

i  racheobronchitis  and,  82 
Meiliast init is  in  lobar  pneumonia,  206 
Melanosis,  284 
Meltzer's    theory    in    bronchial    asthma, 

19 
Meningismus  in  pneumonia,  192 
Meningitis  in  bronchiectasis,  I  1  1 

in  Lobar  pneumonia,  212 
Meningoencephalitis     in    lobar     pneu- 
monia, 212 
Mercury  embolism,  348 

symptoms  of,  348 
Metallic  dust,  284 

tinkle  in  pneumothorax,  573 
Metastatic  sarcoma,  441 
Micrococcus  catarrhalis,  82 
Migratory  pneumonia,  194 
"Miner's  lung,"  277 
Monilia,  392 
Mucopurulent  bronchitis,  101 


N 


Nephritis   in  lobar  pneumonia,   212 
Nervous  system  in  lobar  pneumonia,  212 
Neuritis  in  lobar  pneumonia,  214 
Nocardia,  389 


Obstruction  atelectasis,  130 

causes  of,  130 
Ocular  disturbances  in  lobar  pneumonia, 

214 
O'idiosis,  bronchial,  128 
O'idium,  392 
Oospora,  389 
Organic  dust,  284 

Osteo-arthropathy,  "pulmonary,"  hyper- 
trophic,  bronchiectasis   and,    118 
Otitis  media,  acute,  in  acute  bronchitis,  91 
in  bronchopneumonia,  247 
in   lobar  pneumonia,    215, 
232 


Papilloma  in  bronchi,  22 
Parapleural  echinococcus,  558 
Parapulmonary  echinococcus,  406 
Parasites,  animal,  404 

hemoptysis  from,  355 
Parotitis,  acute,  in  lobar  pneumonia,  211 
Pericarditis  in  bronchiectasis,  114 
in  lobar  pneumonia,  209 


INDEX 


509 


Peripleuritis,  534 
Perisporcaeea,  399 
Peritonitis  in  lobar  pneumonia,  210 
Pertussis  bacillus,  81 
Phagocytic  endothelial  cells,  501 
Phonation  phenomenon,  480 
Phthisis,  aneurysmal,  18 
Plague  pneumonia,  257 
Pleura,  actinomycosis  of,  533 
carcinoma  of,  551 

occurrence  of,  551 
pathology  of,  551 
prognosis  of,  554 
symptoms  of,  553 
synonyms  of,  551 
treatment  of,  554 
condition  of,  in  pulmonary  abscess 

and  gangrene,  296 
diseases  of,  453 
echinococcus  disease  of,  557 
etiology  of,  557 
special  pathology   of,    557 
lipoma  of,  550 
sarcoma  of,  555 
streptothricosis  of,  533,  534 
syphilis  of,  535 
tumors  of,  550 
benign,  550 

malignant,  primary,  551 
secondary,  556 
Pleural  fluids,    chylous   and   chyliform, 
546 
determination  of  character  of, 

498 
examination  of,  499 

bacteriology  in,  503 
chemistry  in,  499 
cytology  in,  500 
hemorrhagic,  539 
Pleuritis,  453 

acute  fibrinous,  459 

blood  in,  464 
cough  in,  462 
diagnosis  of,  464 
dyspnea  in,  462 
etiology  of,  459 
pains  in,  461 
pathology  of,  460 
physical  signs  in,  462 
primary,  459 
prognosis  of,  465 
secondary,  459 
sequela?  in,  464 
site  of,  461 
symptoms  of,  461 
treatment  of,  465 
purulent,  518 

after-treatment  in,  528 
blood  in,  522 
causes  of  death  in,  524 
complications  of,  522 

amyloid    degeneration 

in,  524 
extension  to  neighbor- 
ing  organs   in,    522 


Pleuritis,   acute  purulent,  complications 
of,  metastatic  Lesions  in, 
524 
diagnosis  in,  525 
effusion  in,  520 
etiology  of,  518 
examination  of  pleural  pus 

in,  526 
exploratory  puncture  in, 525 

incision  in,  526 
location  of,  520 
mixed  infections  in,  519 
operation  in,  529 
pathology  of,  520 
physical  signs  of,  521 
pneumococcus  in,  519 
primary  form  of,  518 
prognosis  of,  527 
pulsating  empyema  and, 

521 
relapse  in,  524 
secondary  form  of,   518 
sequelae  in,  525 
staphylococcus  in,  519 
streptococcus  in,  519 
symptoms  of,  521 
treatment  of,  527 

costatectomy  in,  527 
methods  of,  527 
thoracotomy  in,  527 
tubercle  bacilli  in,  519 
tuberculous    empyema    in, 

528 
types  of,  519 
vaccination  in,  528 
serofibrinous,  467 

auscultation  in,  484 
axillary  glands  in,  491 
blood  in,  490 
blood-pressure  in,  491 
causes  of  sudden  death  in, 

493 
complications  in,  492 
diagnosis  of,  494 
diaphragm  phenomenon  in, 

487 
duration  of,  493 
effusion  in,  472 
etiology  of,  467 
heart   in,  displacement  of, 
485 
examination  of,  485 
inspection  in,  480 
palpation  in,  481 
paravertebral    dulness    on 
affected  side  in,  489 
triangle  of  dulness  in, 
488 
pathology    of,    471 
physical  signs  in,  479 
pleura  in,  471 
prognosis  of,  504 
prophylaxis  of,  505 
pupils  in,  491 
radioscopy  in,  491 


600 


INDEX 


Pleuritis,  acute  serofibrinous,  relapse  in. 

494 
sequelae  in,  494 
spleen  in,  491 
symptoms  of,  477 
primary,  477 
•  secondary,  478 
special,  478 
treatment  of,  505 

general    measures    in, 

505       ' 
local    applications    in, 

506 
natural  cure  in,  505 
special    measures    in, 
506 
in  bronchiectasis,  113 
chronic,  535 
classification  of,  458 
diaphragmatic,  531 
dry,  535 
etiology  of,  459 
bacterial,  457 

microorganisms  in,  458 
pneumococcus  in,  458 
streptococcus  in,  458 
tubercle  bacillus  in,  457 
general,  456 
age  in,  456 
exposure  in,  457 
occupation  in,  456 
season  in,  456 
sex  in,  456 
hemorrhagic,  539 
history  of,  453 
infectious,  469 

infection    of    other    parts    in, 

471 
rheumatism  in,  470 
trauma  in,  470 
typhoid  fever  in,  470 
in  lobar  pneumonia,  206 
metapneumonic,  469 
occurrence  of,  455 
plastic,  459 
primary,  459 
secondary,  459 
special  forms  of,  531 
thoracentesis  in,  453 
tuberculous,  467 

animal  inoculation  in,  468 
cells  in,  468 
exudate  in,  468 
postmortem  evidence  in,  468 
subsequent  history  of,  467 
tubercle  bacillus  in  the  fluid  in, 

468 
tuberculin  reaction  in,  468 
tuberculosis    of    other    organs 
and,  467 
with  effusion,  535 
Pleurotomy    in    surgical    treatment    of 
pulmonary  abscess  and  gangrene,  314 
Pneumectomy  in  surgical  treatment  of 
bronchiectasis,  125,  126 


Pneumectomy  in  surgical  treatment  of 
malignant  disease  of 
lung,  445 

of  pulmonary  abscess  and 
gangrene,  315 
Pneumobronchotomy  in  bronchostenosis, 

39 
Pneumococci  in  apparently  healthy  indi- 
viduals, 169 
cultivation  of,  187 
in  non-pulmonary  lesions,  173 
outside  the  body,  169 
toxin  production  of,  170 
Pneumococcus  in  acute  purulent  pleuritis 
519 
animal  experimentation  with,  174 
bacterial  etiology  of,  in  pleuritis,  458 
cultural  peculiarities  of ,  165 
culture,  aerobic,  165 

cover-glass  preparation  of,  166 
Frankel,  165 
morphology  of,  165 
septicemia,  173 
in  sputum,  164 
Pneumohydrothorax,    bronchostenosis 

and,  17 
Pneumonia,  abortive,  196 
alba,  364,  365 
in  alcoholics,  196 
apical,  195 
asthenic,  194 

catarrhal,    245.     See  Bronchopneu- 
monia, 
central,  194 
in  children,  195 

chronic    interstitial    in    bronchiec- 
tasis, 113 
clinical  varieties  of,  194 
diabetes  and,  197 
ether,  196 

in  heart  disease,  197 
hemoptysis  in,  352 
in   hereditary    form    of    pulmonary 

syphilis,  364 
hypostatic,  321 

indurative,  bronchopneumonic  form 
of,  266 
chronic,    subacute   and,    264 
etiology  of,  264 
pathology  of,  265 
diagnosis  of,  272 
displacement  of  viscera  in,  271 
lobar  form  of,  265 
massive  form  of,  265 
physical  signs  of,  270 
prognosis  of,  274 
prophylaxis  of,  275 
symptoms  of,  268 
treatment  of,  275 
insanity  and,  199 
lobar,  157 

abdominal  pain  in,  185 
abscess  in,  182,  206 
accidents  of  resolution  in,  182 
acute  otitis  media  in,  215 


INDEX 


601 


Pneumonia,    lobar,    acute,   parotitis  in, 
211 

age  and,  160 

antitoxin  in,  171 

arthritis  in,  215 

aspiration  and,  161 

autolysis  in,  180 

bacteriology  of,  163 

blood  in,  204 

blood-pressure  in,  189 

bronchitis  in,  205 

bronchopneumonia  in,  218 

carbon-dioxide  content  of  blood 
in,  178 

cardiovascular  system  in,  207 

chemotherapy  of,  224 

circulatory  system  in,  188  . 

coagulation    time    in,    205 

cold  and,  160 

complications  of,  205 

contagiousness  and,  159 

convalescence  in,  233 

cough  in,  186 

crisis  in,  233 

cyanosis  in,  185 

death  in,  221 

delayed  resolution  in,  193 

delirium  in,  192 

diagnosis  of,  216 
differential,  216 

diet  in,  228 

digestive  system  in,  193 

directions  for  nurses  in,  227 

endocarditis  in,  207 
prognosis  of,  208 

epidemics  and,  158 

examination  of  patients   with, 
226 
of  sputum  for  pneumococci 
in,  187 
fever  in,  184 
gangrene  in,  182,  206 
gastro-intestinal  system  in,  210 
general  clinical   description   of, 
183 
considerations  in,  225 
factors  in,  157 
geographic  factor  in,  157 
•    heart  in,  189 
hygienic  management  in,  226 
immersion  in  water  and,  161 
immune  sera  in,  225 
immunity  from,  171 
increased  virulence  of  organism 

and,  158 
incubation  period  of,  182 
individual  factors  in,  160 
inhalation  and,  161 
inorganic  substances  in,  178 
inspection  in,  200 
iodophilia  in,  205 
jaundice  in,  210 
lymph  glands  in,  191 
mediastinitis  in,  206 
meningismus  in,  192 


Pneumonia,  lobar,  meningitis  in,  213 
meningo-encephalitifl  in,  212 
metabolism  in,  176 
meteorologic  factors  in,  158 

nephritis  in,  212 
nervous  system  in,  191,  212 
neuritis  in,  214 
occupation  and,  160 
occurrence  of,  157 
ocular  disturbances  in,  214 
oxygen  content  of  blood  in,  177 
palpation  in,  200 
pathogenesis  of,  176 
pathology  of,  179 
percussion  in,  200 
pericarditis  in,  209 
peritonitis  in,  210 
persistence  of  fever  in,  219 
personal  condition  and,  162 
physical  signs  in,  200 
pleural  exudates  in,  218 
pleuritis  in,  206 
pneumothorax  in,  206 
predisposing  influences  in,  157 
previous  attacks  and,  163 
prodromata  in,  182 
prognosis  of,  219 
age  in,  219 
character  of  organisms  in, 

220 
complications  in,  220 
personal  condition  in,  220 
prophylaxis  of,  222 
pulmonary    abscess    and    gan- 
grene and,  290 
infarction  in,  217 
tuberculosis  and,  162 
pupils  in,  214 
racial  factor  in,  157 
reflexes  in,  214 
respiration  in,  186 
respiratory  symptoms  in,  185 
sex  and,  160 
site  of  disease  in,  181 
skin  in,  190 

special  symptoms  of,  184 
spleen  in,  191 
sputum  in,  186 
subphrenic  abscess  in,  206 
symptoms  of,  183 
tetany  in,  214 
trauma  and,  161 
treatment  of,  224 

special  symptoms,  228-232 
typhoid  fever  and,  162 
urine  in,  190 
vaccines  in,  225 
vascular  lesions  in,  210 
white  cells  in,  204 
x-ray  examination  in,  202 
lobular,     245.     See     Bronchopneu- 
monia. 
malaria  and,  199 
massive,  194 
migratory,  194 


602 


INDEX 


Pneumonia,  plague,  257 

primary,  258 

secondary,  258 
pleurogenous  interstitial,  266 
postoperative,  L96 
in  pregnancy,  L96 
pulmonary  buberculosis  and,  196 
in  renal  disease,  197 
senile,  L94 
terminal,  196 

traclieohroneliitis  and,  83 

typhoid  fever  and,  197 
Pneumonocele,  448 
Pneumonoconiosis,  276 

diagnosis  of,  288 

etiology  of,  279 

foreign  pigment  in  lung  tissues  in, 
282 

history  of,  276 

hit  est  inal  t  heory  in,  278 

origin  of,  276 

pathology  of,  285 

prophylaxis  of,  288 

symptoms  of,  287 

treatment  of,  289 
Pneumothorax,  564 

acutissimus,  579 

artificial,  580 

apparatus  for,  581 
for  bronchiectasis,  126 
dangers  in,  583 
indications  for,  580 
methods  in,  581 
results  in,  584 
theories  for,  580 

closed, 579 

course  of,  587 

diagnosis  of,  584 

double,  580 

etiology  of,  566 

history  of,  564 

incidence  of,  566 

intrapleural  pressure  in,  565 

in  lobar  pneumonia,  206 

open,  578 

partial,  580 

pathologic  physiology  of,  564 

pathology  of,  569 

prognosis  of,  587 

signs  of,  571 

symptoms  of,  570 

treatment  of,  588 

valvular,  579 

varieties  of,  578 

x-ray  examination  in,  577 
Pneumotomy   in   surgical   treatment   of 
pulmonary  abscess  and  gangrene,  314 
Polypi  in  bronchi,  22 
Potain's  apparatus  in  treatment  of  acute 

serofibrinous  pleuritis,  511 
"  Potter's  phthisis,"  284 
Pregnancy,  pneumonia  in,  196 
Pseudochylous  fluids,  546 
Pseudotuberele  bacillus,  389 
Psittacosis,  241 


Psittacosis,  bacteriology  of,  211 

diagnosis  of,  211 

epidemics  of,  242 

pathology  of,  243 
prognosis  of,  2  11 
prophylaxis  of,  2  I  1 
symptoms  of,  243 
treatment  of,  244 
Pulmonary  abscess,  290 
arteriosclerosis,  451 
aspergillosis,  399 
blast  omycosis,  392 
congestion,  318 

diagnosis  of,  321 

prognosis  of,  321 

treatment  of,  321 
disease,  chronic  bronchitis  and,  95 

dust  and,  279 
distomatosis,  420 
echinococcus,  406 
edema,  321 
embolism,  328 
gangrene,  290 
infarction,  328 

in  lobar  pneumonia,  217 
streptothricosis,  389 
syphilis,  364 

theory  in  bronchiectasis,  114 
thrombosis,  328 

tuberculosis,  lobar  pneumonia  and, 
162,  196 
Puncture,  exploratory,  in  abscess,  308 

in  bronchiectasis,  122 

in  echinococcus  disease,  415 

in  empyema,  525 

in  gangrene,  308 

in  indurative  pneumonia,  273 

in  malignant  disease  of  lung,  441 

in  serofibrinous  pleuritis,  498 

in  traumatic  hemothorax,  544 
Pupils  in  lobar  pneumonia,  214 
Purulent  bronchitis,  101 
Putrid  bronchitis,  102 
Pyopneumothorax,  543 


Quinine  in  treatment  of  pneumonia,  224 


R 


Reflexes  in  lobar  pneumonia,  214 
Respiratory  tract,  normal,  bacteriology 

of,  84 
Retraction  atelectasis,  130 
Rheumatism  in  infectious  pleuritis,  470 
Rupture  of  lung,  prognosis  of,  544 


Saccharomyces,  392 
Sarcoma  of  lung,  primary,  432 


INDEX 


603 


Sarcoma  of  lung,    primary,    appearance 
of,  443 
bronchoscopy  in,  442 
diagnosis  of,  440 
etiology  of,  433 
exploratory   puncture   in, 

441 
pathology  of,  433 
physical  signs  of,  435 
prognosis  of,  445 
sputum  in,  438 
symptoms  of,  434 
treatment  of,  445 
rc-ray  examination  in,  440 
metastatic,  441 
of  pleura,  555 
Scleroma  of  bronchi,  28 

bronchostenosis  and,  17 
Senile  pneumonia,  194 
Siderosis  pulmonum,  278 

and  pneumonoconiosis,  284 
Siphon  drainage  for  empyema,  527 
Siphonage  of  pleural  fluid,  509 
Smallpox,  tracheobronchitis    and,    82 
Soot  dust,  284 

Spirochsetse  in  lung  tissue,  367 
in  abscess  of  lung,  297 
in  bronchitis  obliterans,  74 
Sputum  in  abscess,  298 
in  actinomycosis,  381 
in  acute   fibrinous   pleuritis,    462 
pulmonary  edema,  325 
purulent  pleuritis,  522 
serofibrinous  pleuritis,  478 
tracheobronchitis,  69 
in  aspergillosis,  402 
in  blastomycosis,  397 
in  bronchial  asthma,  53 
in  bronchiectasis,  116 
•in  bronchitis,  bacteriology  of,  85 

fibrinosa,  70 
in  bronchopneumonia,  254 
in  cardiac  asthma,  321 
Charcot-Leyden  crystals  in,  47,  55 
Curschmann  spirals  in,  48,  53 
in  distomatosis,  424 
in  echinococcus  disease  of  lung,  408 
409 
of  pleura,  559 
in  emphysema,  146 
in  fat  embolism,  348 
in    Friedlander's    bacillus    pneu- 
monia, 239 
in  gangrene  of  lung,  301 
in  hemoptysis,  352 
in  infarction  of  lung,  339 
influenza  bacilli  in,  78 
in  lobar  pneumonia,  186 
in  malignant  tumors  of  bronchi,  437 

of  lung,  437 
in  passive  congestion  of  lung,  320 
in  plague  pneumonia,  257 
in  pneumonoconiosis,  287  ' 
in  psittacosis,  243 
in  streptothricosis  of  lung,  390 


Sputum  in  syphilis  of  lung,  368 

of  I  rachea  and  bronchi,  24 
Staphylococcus  in  acute  purulent    pleu- 
ritis, 519 
"Stasis  catarrh,"  94 
"Steel  grinder's  phthisis,"  284 
Stenosis    of    large    and    medium-sized 
bronchi,  17 
syphilitic,    bronchiectasis    and,    122 
"Stone  asthma,"  41 
dust,  284 

"mason's  phthisis',"  284 
Streptococcus  in  acute  purulent  pleuritis, 
519 
in  bacterial  etiology  of  pleuritis,  458 
mucosus  capsulatus,  aerobic  culture 
of,  167 
cover-glass  preparation  of, 

168 
in  pneumonic  exudate,  168 
in  sputum,  166 
stab-culture  of,  167 
Streptothricosis  of  pleura,  533 
pulmonary,  389 

diagnosis  of,  390 
etiology  of,  389 
microorganisms  of,  389 
pathology  of,  390 
prognosis  of,  391 
symptoms  of,  390 
treatment  of,  391 
Streptothrix,  389 
Strongyloides,  426 
Strongylus  longevaginatus,  426 
Subdiaphragmatic    abscess    complicated 
by  pleurisy,  82 
of  the  right  side,  496 
Subphrenic  abscess  in  lobar  pneumonia, 

207 
Succussion  sound  in  pneumothorax,  574 
Syphilis  of  bronchi,  23 
diagnosis  of,  26 
pathology  of,  24 
prognosis  of,  27 
signs  of,  24 
symptoms  of,  24 
treatment  of,  27 
bronchiectasis  and,  110,  122 
bronchostenosis  and,  17 
chronic  bronchitis  and,  96 
congenital    pulmonary  tuberculosis 

and,  relation  of,  366 
of  pleura,  535 
pulmonary,  364 
acquired,  366 

diagnosis  of,  368 
pathology  of,  367 
physical  signs  of,  368 
prognosis  of,  370 
symptoms  of,  368 
treatment  of,  370 
congenital,  364 

gummata  in,  364 
pneumonia  in,  364 
of  treachea,  23 


G04 


INDEX 


Syphilis  of  treachea,  diagnosis  of,  26 
pathology  of,  26 

prognosis  of,  27 
signs  of,  24 
symptoms  of,  24 
treatment  of,  27 
tracheobronchitis  and,  82 


Telangiectatic  broehiectasis,  126 
Terminal  pneumonia,  196 

Tetany  in  lobar  pneumonia,  214 
Thoracentesis  in  carcinoma  of  pleura,  554 
in  chylothorax,  548 
in  pleuritis,  453,  506 
in  pneumothorax,  567,  589 
in  traumatic  hemothorax,  545 
Thoracotomy   in   surgical  treatment   of 
pulmonary  abscess  and  gangrene, 
313 
in    treatment    of    acute    purulent 
pleuritis,  527 
of  pneumothorax,  589 
Thrombosis,  pulmonary,  328 
diagnosis  of,  341 
etiology  of,  328 
occurrence  of,  328 
pathology  of,  332 
prognosis  of,  343 
treatment  of,  343 
Tobaccosis,  285 

Trachea,  lesions  of,  hemoptysis  in,  354 
syphilis  of,  23 
tuberculosis  of,  27 
Tracheobronchial     glands,     results     of 

changes  in,  286 
Tracheobronchitis,  acute,  77 
auscultation  in,  90 
classification  of,  77 
complications  in,  91 
course  of,  92 
diagnosis  of,  91 
etiology  of,  77 
infection  in,  77 
influenza  and,  78 

bacilli  in  sputum  of,  78 
inspection  in,  89 
pathology  of,  87 
palpation  in,  90 
percussion  in,  89 
prognosis  of,  92 
prophylaxis  of,  93 
signs  of,  89 
symptoms  of,  88 
treatment  of,  93 
anthrax  and,  83 
diphtheria  and,  83 
diphtheroid  bacilli  in,  81 
erysipelas  and,  83 
glanders  and,  83 
malaria  and,  83 
measles  and,  82 
mechanical  causes  in,  84 


Tracheobronchitis,  pneui lia  and,  83 

smallpox  and,  82 

syphilis  and,  82 
toxic  causes  in,  84 
tuberculosis  and,  83 
typhoid  fever  and,  82 
typhus  fever  and,  S2 
variola  and,  83 
whooping  cough  and,  SI 
Tracheotomy,  intrathoracic,  in  broncho- 
stenosis, 38 
Trauma  in  infectious  pleuritis,  470 
Trocar  for  thoracentesis,  507 
Tubercle  bacilli  in  abscess  or  gangrene, 
292 
in     acute    purulent     pleuritis, 

519 
in  bacterial  etiology  of  pleuritis, 

457 
differentiation  of,  from  strepto- 

thrix,  391 
in  pleural  fluid,  after  artificial 
pneumothorax,  583 
pus,  526 
in    serofibrinous    pleural    effu- 
sions, 468,  504 
Tuberculin  reaction  in  tuberculous  pleu- 
ritis, 468 
Tuberculosis,  acute  of  lung,  diagnosis  of, 
from  pneumonia,  216 
of  bronchi,  27 

diagnosis   of,  from   syphilis   of 
bronchi,  27 
of  bronchial  glands,   chronic  bron- 
chitis and,  97 
bronchiectasis  and,    109,    111,    121, 

prognosis  of,  122 
bronchitis  and,  diagnosis  of,  103 
bronchostenosis  and,  17 
cause     of     indurative     pneumonia, 

diagnosis  of,  273 
chronic  bronchitis  and,  95 

symptoms  of,  99 
comparison  of  pathology  of  blasto- 
mycosis to  395 
development    of,    after    empyema, 

538 
diagnosis  of,  from   abscess  or  gan- 
grene, 305 
fibrinous  bronchitis  and,  66 
inhalation  of  dust  and,  279,  281 
of    mediastinal    glands,     chronic 

bronchitis  and,  97 
miliary,  after  hemoptysis,  360 
chronic  bronchitis  and,  95 
diagnosis     of,    from    broncho- 
pneumonia, 260 
resemblance  of  bronchitis  oblit- 
erans to,  75 
osteo-arthropathy  and,   118 
pleural,  spontaneous  cure  of,  505 

treatment  of,  505 
pneumonia  and,  196 
pulmonary,  acute  tracheobronchitis 
and,  83 


INDEX 


605 


Tuberculosis,  pulmonary,   bronchitis  as 
complication    of,    symptoms 
of,  99 
bronchopneumonia  and,  247 
bronchostenosis  and,  18 
cause  of    bronchiectasis,    diag- 
nosis of,  121 
chronic  bronchitis  and,  95 
death  rate  from,  280 
diagnosis   of,  ■  from    actinomy- 
cosis, 384 
from      bronchopneumonia, 

260 
from  echinococcus  disease 

of  lung,  416 
from  emphysema,  149 
from  malignant  disease  of 

lung,  443 
from     pulmonary     blasto- 
mycosis, 397 
distomatosis,  425 
infarction,  342 
syphilis,  369 
hemoptysis  in,  352,  357 
lobar  pneumonia  and,  162 
pneumothorax  and,  566 

prognosis  of,  587 
prognosis    of,    compared    with 

actinomycosis,  385 
relation  of  emphysema  to,  149 
resemblance  of  aspergillosis  to, 

402 
thrombosis  and,  330 
relation  of  empyema  at  autopsy  to, 
520 
of  hemorrhagic  pleurisy  to,  539 
of  primary  fibrinous  pleuritis  to, 

459 
of  serofibrinous  pleuritis  to,  467 
of  traumatic  hemothorax  to,  542 
of  ribs,  diagnosis  of,  from  actinomy- 
cosis, 385 
of  trachea,  27 
tracheobronchitis  and,  83 
treatment     of     primary     fibrinous 
pleurisy  as  manifestation  of,  466 
Tuberculous  empyema,  treatment  of,  528 

pleuritis,  467 
Tumors  of  bronchi,  22,  427 

bronchiectasis  and,  110 
of  lung,  427 

malignant,  bronchostenosis  and,  17 
mediastinal,  bronchiectasis  and,  110 
of  pleura,  550 


Typhoid  fever,    infectious    pleuritis    in, 
470 
lobar  pneumonia  in,  162,  197 
tracheobronchitis  and,  82 

Typhus  fever,  tracheobronchitis  and,  82 


Uncinaria,  426 
Universal  bronchiectasis,  126 
Urticaria  after  removal  of  pleural  fluid, 
515 


Vaccination  for  empyema,  528 
Variola,  tracheobronchitis  and,  83 


W 


Weigert's  elastic  tissue  stain,  299 
White  cells  in  lobar  pneumonia,  204 

pneumonia,  364 
Winter  cough,  cause  of,  95 
Whooping     cough,     bronchopneumonia 
and,  257 
in  tracheobronchitis,  81 
Woillez's  disease,  318 
Wounds  of  lung,  treatment  of,  545 


X-rays  in  abscess,  307 
in  atelectasis,  137 
in  blastomycosis,  398 
in  bronchiectasis,  122 
in  bronchostenosis,  21 
in  echinococcus  disease  of  lung,  413 
in  emphysema,  148 
for  foreign  bodies,  33,  42 
in  gangrene,  307 
in  lobar  pneumonia,  202 
in  malignant  disease  of  lung,  440, 

445 
in  pneumothorax,  577 
in  pulmonary  arteriosclerosis,  452 
in  serofibrinous  pleuritis,  491 
in  syphilis  of  trachea  and  bronchi,  27 


T 


Vievd 


I 


HhhB 

ISSSI 

